UMEM Educational Pearls - Cardiology

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.

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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.]

Syncope patients are often misdiagnosed as having a seizure. Some factors favoring true syncope:
1. Preceding nausea or diaphoreses
2. Oriented (not confused) upon waking (no post-ictal period).
3. Age > 45
4. Prolonged sitting or standing before episode
5. History of CHF or CAD

Factors favoring seizures:
1. History of seizure disorder
2. Tongue biting
3. Confusion upon waking
4. Loss of consciousness > 5 min
5. Age < 45
6. Preceding aura
7. Observed unusual posturing, jerking, or head turning during episode

Amiodarone-induced hypothyroidism is well-reported and should be considered anytime a patient that chronically takes amiodarone presents with hypothyroid symptoms, including decompensated CHF, decreased mental status, or myxedema coma (e.g. bradycardia, hypotension, hypothermia). 

Other drugs that have been implicated in producing hypothyroidism include lithium, iodine, iodinated contrast, and sulfonamides.

An estimated 20-30% of patients with ACS end up having no identifiable culprit lesion on angiography. Almost half of these patients have inducible coronary spasm. Although these patients have a good outcome, they also have a tendency to return to the hospital for frequent re-evaluations. Evaluation for and treatment of spasm can improve the quality of life for these patients and also to decrease re-visits.

When patients with reports of "clean" coronaries return to the ED with a concerning presentation for ACS, one of the considerations should be coronary spasm. Consider prompting the primary care physician or admitting team to look into this possibility, as it may result in a reduction in recurrent ED visits.

 

 

Severe emotional stress is well-reported to produce an unusual transient cardiomyopathy that mimics cardiac ischemia or infarction on ECG as well as biomarker testing. On angiography, the coronaries are often clean. The ventriculogram takes on an apical or mid-ventricular ballooning appearance due to akinesis. In the ED, these patients will look just like a real thrombosis-related case of ACS and they often develop cardiogenic shock. Unlike true AMI-related cardiogenic shock, these patients have an excellent prognosis...if treated aggressively early-on with supportive therapy (e.g. pressors).

Intracranial catastrophes, such as hemorrhage, ischemic stroke, and head trauma; and severe medical illnesses, such as sepsis, pheochromocytoma, and catecholamine-excess states, are also reported to produce a similar syndrome of LV dysfunction.

The takeaway points: (1) severe emotional stress can be deadly...be wary of diagnosing "anxiety" or "panic attack" without checking an ECG; (2) check an ECG early in the course of any patients with the above conditions that look sick; (3) if the ECG shows signs of severe ischemia, aggressive treatment can be life-saving.

[ref: Bybee KA, Prasad A. Stress-related cardiomyopathy syndromes. Circulation 2008;118;397-409.]

 A normal ECG should not be a huge source of relief when evaluating patients with possible or confirmed myocardial infarction. 8% of acute myocardial infarctions have a completely normal ECG at the time of presentation, and these patients have a 5.7% in-hospital mortality. Serial electrocardiography can certainly improve the yield of electrocardiography but does not rule out AMI with 100% accuracy.

Like most tests in medicine, the ECG is very useful at ruling in disease, but it is limited at ruling out disease.

[The Prognostic Value of a Normal or Non-specific Initial ECG in AMI. JAMA 2001.]
 

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.]