EKG of the Week Question and Solution – Week 15
78 F with h/o DM, and HTN presents with SOB and cough for 2-3 weeks. Pt was seen at UCC and diagnosed with new onset afib with RVR and new onset CHF prior to being transferred to SAMMC. Pt denies CP, syncope, diaphoresis. Here are her EKGs:
CODE stemi called on patient. For ST elevation in inferior leads in II, III, and aVF. Pt went to CATH lab, remained stable while in ER.
Following findings during her workup.
ECHO:
Left Ventriculography:
1. Preserved LV function with LVEF 45-50%.
2. Mid to distal inferior wall hypokinesis.
3. Basal inferior wall akinesis with true aneurysm.
4. Normal LVEDP measured at 15mmHG.
5. No aortic valve stenosis by pullback gradient.
Angiography
Conclusions:
1. Distal left main 50-60% stenosis involving trifurcation with medina (1,0,0,0).
2. Proximal RCA complex ulcerated severe 90% stenosis.
3. Preserved LV function with LVEF 45-50%.
4. Mid to distal inferior wall hypokinesis.
5. Basal inferior wall akinesis with true aneurysm.
6. Normal LVEDP measured at 15mmHG.
7. No aortic valve stenosis by pullback gradient.
–No stent placed pt scheduled for CABG.
Big learning point for this case for me:
Pt denied chest pain since onset of dyspnea. When the Cardiology team came down, the 3rd year IM resident looked at the EKG and said “well she’s not having chest pain so why did you call a code stemi? We talk about atypical chest pain or chest pain equivalents quite often in the ER, but this case really illustrated that to me.
This is an awesome article about missed MIs in the ER, particularly this section:
1) Patient factors:
First, not all patients with MI have chest pain. Up to 1/3 of patients will have silent or atypical symptoms such as shortness of breath, malaise, fatigue, pre-syncope/syncope, or nausea/vomiting.9,10 The Global Registry of Acute Coronary Events (GRACE) trial found 8.4% of patients did not have chest pain, and dyspnea was actually the dominant symptom in more than half of patients.3 Females, older patients, diabetics, and patients with heart failure more often present atypically. Unfortunately, those patients who present atypically often receive suboptimal treatment and have increased morbidity and mortality. Mortality has been shown to be 13% in those presenting with atypical symptoms as compared to 4% presenting with typical symptoms.
Traditional factors are for population use only and not for individual patients
The presence of classic cardiac risk factors such as hypertension, smoking, hyperlipidemia, and diabetes are helpful for predicting long-term risk of coronary artery disease (CAD) in a population, but they are limited in ruling out ACS. If the story is good for ACS but the patient has no risk factors, clinicians should still consider it as a diagnosis. One study demonstrated that 10.5% of patients with non-STEMI had none of the traditional risk factors. A separate study by Body showed that 12% of patients with no risk factors ruled in for acute MI. In younger patients who died of “non-natural causes” with average age of 36 years, over 80% of patients had coronary disease at autopsy, with 8% having significant coronary obstruction.13 Thus, be wary of discounting ACS risk based on patients with no classic risk factors or just because the patient is young!1\
Consider nontraditional risk factors in younger patients with chest pain. Patients with HIV/AIDS have higher risks of MI due to HAART therapy and chronic inflammation, which both can cause increased thrombus and platelet plug formation. In particular, protease inhibitors may cause hyperglycemia, hyperlipidemia, and central obesity.A higher prevalence of hyperlipidemia, arteriosclerosis, left ventricular hypertrophy, and heart failure are also present in patients with chronic kidney disease. Dialysis patients have a 10 to 30 times higher mortality from coronary disease as compared to the general population. Lupus is another important risk factor, as women with lupus aged 35 to 44 years have 50 times greater risk of MI. The mean age of lupus patients with first MI is 20 years younger than those without lupus. This disease causes premature atherosclerosis due to chronic steroid use, inflammation, hyperlipidemia, and renal disease.17 Long-term steroid use is itself a risk factor due to increased insulin resistance, hyperlipidemia, central obesity formation, and hypercoagulability. Pregnancy is also a risk factor for acute MI, with risk increased four-fold. This risk is even higher in women over 40 years (30 fold risk). Heart disease is now one of the largest non-obstetric related causes of death in pregnant women in the developed world.
Elderly patients present several challenges for emergency physicians. They often present atypically with dyspnea, fatigue, and/or nausea with vomiting. Chest pain is present in 50% of cases of MI in the elderly. They are also less likely to have diagnostic ECGs, with ST depression and/or subtle changes more common. The proportion of patients over 85 years with NSTEMI who have non-diagnostic ECG is over 40%! Baseline abnormalities are often present on the ECG including left bundle branch block (LBBB), paced rhythms, left ventricular hypertrophy, and prior MI. Due to the often atypical presentations and non-diagnostic ECGs, the elderly are at tremendous risk of death from MI due to under diagnosis and under treatment. The 30-day mortality after MI in patients less than 65 years is 3%, 65-74 years 10%, 75-84 years 20%, and over 85 years 30%. Elderly patients account for over 80% of deaths from MI. The older patient warrants a closer evaluation for ACS.
Beware of the patient presenting with anxiety and recent emotional events. These patients are at higher risk of ACS, as a stressful event effectively functions as a stress test. An ECG should be obtained in the anxious patient, especially if he or she has chest pain. Wars, earthquakes, sport games, family arguments, or even road rage can all increase catecholamine release, which may result in unstable plaque rupture and platelet aggregation.
The physical exam for patients with chest pain is important. Always consider other chest pain causes (pulmonary embolism (PE), pneumothorax, esophageal rupture, pericarditis, myocarditis, pneumonia, tamponade, and aortic dissection). Pain that radiates to the bilateral shoulders or right shoulder, chest pain with exertion, chest pain with diaphoresis, and chest pain with nausea/vomiting increase the likelihood of ACS. Chest pain described as pressure surprisingly does not increase the likelihood of ACS. Factors that decrease the likelihood include pleuritic pain, positional pain, sharp pain, pain at rest, and reproducible pain. However, none of these will rule out ACS, as up to 16% of patients with ACS will have atypical pain. For example, 20% of patients have upper abdominal pain or reflux symptoms instead of chest pain. One third of patients have pressure, while 20% will call the pain indigestion. Only 1/3 of patients have pain with exertion, 8% have pain with eating, and 7% have pain with emotional stress. Anywhere from 30% to 50% will have no chest pain. ACS can and will present atypically. You cannot rule out ACS based on the absence of typical symptoms and signs.
One of the most common misdiagnoses in cases of missed MI is reflux esophagitis. Up to 20% of patients present with “indigestion” or “burning” pain.Almost 50% of patients with acute MI report increase in belching, 15% obtain some relief with antacids, and 7% obtain complete relief with antacids. Do not use a gastrointestinal (GI) cocktail as a diagnostic tool. Patients with documented coronary disease and those without have similar pain relief from GI cocktails. An Annals of Emergency Medicine study demonstrated that patients with chest pain and abdominal pain had similar frequencies of responses to GI cocktails.26 If you are going to use a GI cocktail to treat a patient’s pain, then know that it should not be used for diagnosis! Before you discharge a patient with “reflux,” consider ACS.
Women experience higher mortality rates and more adverse outcomes, even with less obstructive disease. Women actually have more coronary remodeling of vessels, which means plaques grow into the vessel wall, causing bulging outward. Coronary angiography often misses these lesions. Women will more often have false negative stress tests and angiograms (that will show normal or non-significant disease). Do not rely on stress testing or angiography in these patients.