UMEM Educational Pearls - Cardiology

Three groups of patients are at especially high risk of bleeding from excessive anticoagulation with renally-excreted medications: women, the elderly, and patients with chronic renal insufficiency. For all of these patients, ALWAYS dose their renally-cleared medications based on creatinine clearance, NOT just the creatinine.

Which medications in ACS does this apply to?--enoxaparin and G2B3A inhibitors are the most prominent here to consider.

The literature not only demonstrates increased bleeding complications but also increased MORTALITY if you don't dose based on creatinine clearance!

Although supplemental oxygen has long been considered standard care for patients with ACS, the evidence supporting this concept is largely based on animal studies in which acute MI was artificially induced. Should these studies be extrapolated to humans? Maybe not....


Further review of the animal and human literature actually indicates that the routine use of supplemental oxygen and induction of hyperoxia can actually induce adverse hemodynamic consequences such as increased coronary artery tone and reduction in coronary artery blood flow; reductions in cardiac output and increased systemic vascular resistance; and potentially increased infarction size. It certainly seems prudent to treat hypoxia, but if the patient is not hypoxic, skip the supplemental oxygen!

Wijesinghe M, et al. Routine use of oxygen in the treatment of myocardial infarction: systematic review. Heart 2009;95:198-202.
AND
Farquhar H, et al. Systematic review of studies of the effect of hyperoxia on coronary blood flow. Am Heart J 2009;158:371-377.

A recent study of nearly 800 patients with chest pain evaluated symptoms and signs that are most predictive of ruling in for ACS. The following characteristics made acute MI more likely (likelihood ratios in parentheses): observed diaphoresis (5.18), central location of chest pain (3.29), associated vomiting (3.50), radiation of the pain to bilateral arms (2.69), and radiation of pain to the right arm (2.23).

As we've said before, if your patient sweats, it ought to make YOU sweat!

[BodyR, et al. Resuscitation 2010;81:281-286.]

Major and minor clinical prognostic predictors for pericarditis have been described as follows:

Major: fever > 38 degrees C, subacute onset, large effusion, tamponade, lack of response to aspirin or NSAIDs after at least 1 week of therapy

Minor: myopericarditis, immunodepression, trauma, oral anticoagulant therapy

Patients with any of these criteria [major or minor] should strongly be considered for admission. In the absence of these factors, studies show that patients managed as outpatients do well.

[Imazio M, Spodick DH, Brucato A, et al. Controversial issues in the management of pericardial diseases. Circulation 2010;121:916-928.]


 

Many cardiac patients take warfarin...no surprise.
Many patients use herbal supplements...no surprise.
Many herbal supplements can produce increased bleeding risk with warfarin, and some produce decreased effects of warfarin...that may be a bit of a surprise. Here's a few that are worth knowing:

Herbals that increase the bleeding risk of warfarin: alfalfa, angelica (dong quai), bilberry, fenugreek, garlic, ginger, and ginkgo

Herbals that decrease the effect of warfarin: ginseng, green tea

In addition to asking your patients about their prescription medications, specifically ask your patients if they take herbal supplements, over-the-counter products, or green tea (since many patients don't consider green tea to be either an herbal supplement)...especially if the patient takes warfarin. You just might diagnose or prevent a disastrous bleeding complication.

[Tachjian A, Maria V, Jahangir A. Use of herbal products and potential interactions in patients with cardiovascular diseases. J Am Coll Cardiol 2010;55:515-525.]

Missed cases of ACS account for 10% of all malpractice cases in emergency medicine, yet account for 30% of all the money emergency physicians pay out in malpractice cases. This misdiagnosis is the biggest cause of monetary payout in the specialty.

Three main themes account for the majority of missed cases of ACS:
1. Failure to recognize atypical presentations (e.g. dyspnea)
2. Failure to recognize high-risk groups (e.g. women, diabetics)
3. Over-reliance on negative tests (e.g. negative troponin or recent stress test)

Women are more likely to be misdiagnosed than men when they present with acute coronary syndromes. There are several possible reasons for this:
1. Women are more often older and more often have diabetes, both of which are factors involved in atypical presentations.
2. Women present with chest pain less often than men. On the other hand, women are more likely to present with nausea, vomiting, indigestion, malaise, loss of appetitie, or syncope than men.
3. When women do have chest pain, they are more likely to report pain that has atypical features, such as radation to the right arm or shoulder, front neck, or back; and the pain is more often described as sharp, stabbing, or tansient.

The bottom line is something that I've believed since high school: women are confusing...!

[the references for this ACS information comes from many different sources, but if anyone needs a good review on this topic, just email me: amattu@smail.umaryland.edu]

Most people know that the ECG is only diagnostic of ACS approximately in 50% of cases, and in fact patients presenting with ACS can have an initially completely normal ECG in up to 10% of cases. However, traditional teaching is that if the patient is actively having chest pain or other concerning symptoms, the patient with ACS will nearly always have ECG abnormalities. NOT SO, according to a recent study. Researchers from Davis medical center evaluated patients with presumed ACS and normal ECGs, comparing the prevalence of ACS in patients with active symptoms (e.g. chest pain) during the normal ECG vs. patients that were asymptomatic at the time of the ECG. Cutting to the chase, they found no difference in ther rule-in rate between the two groups. In other words, don't be reassured at all if a patients has a normal ECG during symptoms.

This study supports other studies which continually show that an abnormal ECG is excellent at ruling-in disease, but a normal ECG is poor at ruling-out disease. In the absence of a diagnostic ECG, it's all about the HPI, the HPI, and the HPI. And also...the HPI.

[Turnipsee SD, Trythall WS, Diercks DB, et al. Frequency of acute coronary syndrome in patients with normal electrocardiogram performed during presence or absence of chest pain. Acad Emerg Med 2009;16:495-499.]


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Though most people know that therapeutic hypothermia is indicated in resuscitated victims of cardiac arrest, is it safe if that cardiac arrest victim is also being treated for STEMI? Do you need to worry about increased bleeding complications in these patients that are receiving anticoagulants, lytics, PCI, or other standard "bleeding" medications? Are these patients at increased risk for hemodynamic instability with therapeutic hypothermia?

Recent studies have demonstrated that therapeutic hypothermia in acute MI patients receiving other standard treatments (i.e., anticoagulants, etc.) is SAFE: it is associated with no increase in bleeding complications (1), no increase in time to balloon inflation (2), and no increase in hemodynamic instability or malignant arrhythmias (3).

1. Schefold JC, et al. Mild therapeutic hypothermia after cardiac arrest and the risk of bleeding in patients with acute myocardial infarction. Int J Cardiol 2009;132:387-391.
2. Knafelj R, Radsel P, Ploj T, et al. Primary percutaneous coronary intervention and mild induced hypothermia in comatose survivors of ventricular fibrillation with ST-elevation acute myocardial infarction. Resuscitaiton 2007;74:227-234.
3. Wolfrum S, Pierau C, Radke PW, et al. Mild therapeutic hypothermia in patients after out-of-hospital cardiac arrest due to acute ST-segment elevation myocardial infarction undergoing immediate percutaneous coronary intervention. Crit Care Med 2008;36:1780-1786.

  Despite the traditional use of intravenous medications such as vasopressors and antiarrhythmics for victims of cardiac arrest, there is actually very little evidence to support these therapies. On the contrary, 2 recent multicenter center studies demonstrated that the use of intravenous medications that are advocated in standard advanced cardiac life support (ACLS) guidelines are ineffective at improving survival to hospital discharge of patients with primary cardiac arrest. In contrast, these medications have been shown to increase hospital admissions, bed and resource utilization, and costs. The only interventions that have been shown to improve meaningful outcomes are rapid defibrillation for shockable rhythms, good compressions, post-resuscitation therapeutic hypothermia, and there's increasing evidence for post-resuscitation cardiac catheterization as well.

In other words, the best thing you can do early for patients with primary cardiac arrrest is to focus on the basics.

 

Show References

Although we tend to "shotgun" when ordering labs in elderly patients with syncope, the literature actually indicates that we can be very selective in testing with this group, letting the history and PE determine whether any tests are indicated. The most recent literature supporting this concept demonstrated that even cardiac enzyme testing and head CTs in elderly syncope patients were helpful in only 0.5% of cases. The only test that should routinely be obtained is the ECG...a good history and PE should be sufficient to determine when any other tests are indicated.

[Mendu, et al. Yield of diagnostic tests in evaluating syncopal episodes in older patients. Arch Intern Med 2009]

Yet another publication demonstrates that chest pain radiating to the right arm has the highest predictive value for ruling in ACS. In this study, radiation of the pain to the right arm had a higher predictive value than age, gender, comorbidites or traditional risk factors, specific descriptors of pain (e.g. "pressure" or "crushing"), or associated symptoms (e.g. diaphoresis, nausea, dyspnea). The bottom line....beware chest pain that radiates to the right arm!

[Goodacre S, Pett P, Arnold J, et al. Clinical diagnosis of acute coronary syndrome in patients with chest pain and a normal or non-diagnostic electrocardiogram. Emerg Med J 2009;26:866-870.]

When patients present with acute MI, all NSAIDS should be discontinued (e.g. ibuprofen, COX-2 inhibitors, etc.) during the hospitalization. Continued use of NSAIDs during the hospitalization increases the risk of CHF, myocardial rupture, hypertension, reinfarction, and mortality.

 Myocardial infarctions involving the left circumflex artery are often associated with ECGs that lack any ST-segment changes (38% in one representative study). Oftentimes when there are ST-changes, there may simply be anterior lead ST-segment depression. In these patients, acquisition of a few posterior leads frequently demonstrates STEMI. Some data does exist that failure to diagnose these posterior STEMIs (e.g. simply diagnosing anterior "ischemia" rather than posterior "STEMI") results in increased mortality.

So what's the bottom line?
1. In patients with isolated anterior lead ST-segment depression, always check for posterior STEMI with a couple of posterior leads.
2. In patients with non-significant ECGs but concerning persistent symptoms, always check for posterior STEMI with a couple of posterior leads.

This is always a great time to use that 80-lead ECG if your ED has one.

Amal

During this season of the ever-present viral respiratory illness, we must be on the lookout for the potentially-deadly -entity of myocarditis. A recent study suggests some clues to when the diagnosis should more strongly be considered in patients presenting with viral respiratory symptoms.

1. Most cases of myocarditis were not initially recognized by primary care MDs or emergency health care providers. 84% of patients needed more than one visit within 2 weeks before the diagnosis was made. This highlights the difficulty in Dx and frequent misdiagnosis rate.
2. The most common presenting symptom was dyspnea (69%) and most common sign was tachypnea (60%).
3. Although resting tachycardia is often taught as a common finding, 66% of patients had a normal HR.
4. The most helpful findings in terms of helping distinguish myocarditis from benign common viral URIs was hepatomegaly (present in 50%) and cardiomegaly (present in 60%).
5. An abnormal ECG was present in 100% of cases. The most common abnormalities were tachycardia, ventricular hypertrophy, and ST or T wave changes.
6. 54% of patients had elevated troponin levels.

So what's the bottom line?
1. If your patient has tachypnea or dyspnea, strongly consider getting a CXR. In that case, look carefully for cardiomegaly.
2. Always assess for and document the presence or absence of hepatomegaly.
3. A completely normal ECG is strong evidence against myocarditis.

[Durani Y, Egan M, Baffa J, et al. Pediatric myocarditis: presenting clinical characteristics. Am J Emerg Med 2009;27:942-947.]

Increasing literature has demonstrated that patients post-cardiac arrest benefit from induced hypothermia (IH). In addition, increasing literature has demonstrated that patients with cardiac arrest associated with STEMI are best treated with rapid percutaneous intervention (PCI) after their resuscitation. But what about the combination of IH + PCI in resuscitated cardiac arrest patients with STEMI?

There's now growing support for this concept as well. Wolfrum et al. demonstrated an improved mortality at 6 mos. (35% vs. 25%) in patients that had the combination of IH + PCI vs. patients receiving PCI alone after cardiac arrest and they also had better neurological outcomes.

Next time you have a STEMI patient that has a cardiac arrest who you resuscitate, talk to your cardiologists about the literature demonstrating the improved outcomes with combination IH plus PCI.

[Wolfrum S, Pierau C, Radke PW, et al. Mild therapeutic hypothermia in patients after out-of-hospital cardiac arrest due to acute ST-segment elevation myocardial infarction undergoing immediate percutaneous coronary intervention. Crit Care Med 2008;36:1780-1786.]

The recent Baltimore City Marathon served as a nice reminder in a few cases that long-distance running and other ultra-endurance events can produce elevations in troponin levels. To review the non-cardiac-disease causes of troponin elevations:

sepsis, PE, COPD, carbon monoxide, intracranial abnormalities (including SAH, stroke, IC hemorrhage, seizures), ESRD, rhabdomyolysis, eclampsia and preeclampsia, extreme endurance exercises, UGI bleeding, LVH, catecholamine toxicity 

Severe mitral regurgitation (MR) after MI, accompanied by cardiogenic shock carries a poor prognosis.

Severe MR in many cases is due to infarction of the posterior papillary muscle, and in these cases the area of infarction tends to be less extensive than in those with MR due to severe left ventricular dysfunction. 

Take Home Pearl:

The presence of pulmonary edema and/or cardiogenic shock in a patient with an inferior STEMI should prompt consideration for acute MR due to papilary muscle rupture. Get an echo as fast as you can to confirm or r/o the diagnosis. Treatment is afterload reduction, inotropic support, and urgent surgical repair. 

Don't forget about pheochromocytoma as a possible cause of severe hypertension...especially in those patients that are recalcitrant to "normal" medications. A few important points:
1. Incidence may be as high as 0.2% of patients with hypertension...sounds very rare, but statistically we'll all see some during our career.
2. Mortality may be as high as 10% if unrecognized; but if recognized and treated, excellent prognosis.
3. Suspect this in patients with intermittent episodes of flushing, palpitations, diaphoresis, headaches, and hypertension.
4. Treatment with beta blockers alone (including labetalol) may induce unopposed alpha-activity and worsen BP.
5. Treat with nitroprusside or phentolamine (an alpha blocker). Phentolamine is 5 mg IV, can be repeated every 5-10min as needed.
6. After phentolamine is given, there may be reflex tachycardia. NOW you can add beta blockers.

The most important thing is to keep the diagnosis in mind. It's out there! But you'll miss 100% of the diagnoses you don't consider.

Systemic lupus erythematosus produces a significant predisposition towards premature atherosclerosis. Although the exact mechanism for what causes this is uncertain, premature CAD is at least partially (or largely) caused by systemic inflammation, which can produce endothelial damage and initiates the process of atherogenesis.

The literature indicates that there is a 9X increased risk of CAD in patients with lupus, and the risk increases to 50X higher in women 35-44 years of age! In general, patients with lupus develop their first MI 20 years earlier than age-matched non-lupus counterparts. 

[Mattu A, Petrini J, Swencki S, et al. Premature atherosclerosis and acute coronary syndrome in systemic lupus erythematosus. Am J Emerg Med 2005;23:696-703.]