A 35-year-old-patient with no past medical history comes to the Emergency Department with complaints of several days of fatigue and constant chest pain that is substernal but not radiating, “sharp,” and worsened with inspiration, but seems to improve with sitting forward. He has noticed a 10 lbs unintentional weight gain over the past 2 weeks and significant fatigue. He reports only local travel in the last 2 months and otherwise had a “cold a few weeks ago.” His family history is negative for ischemic heart disease, and he is a nonsmoker and has never used any substances such as cocaine, marijuana, or amphetamines. Examination in the Emergency Department reveals tachycardic heart without gallop or rub, and symmetric 2+ pitting edema to his calves. Initial laboratory test results are notable for an elevated troponin-T and the following ECG:
Which of the following is the BEST imaging modality to diagnose the etiology of his underlying disease?
Correct Answer: B
The presentation is most consistent with viral myocarditis. Diagnosis of myocarditis is multimodal, though the gold standard is considered to be endomyocardial biopsy (EMBx). However, because of the morbidity associated with an EMBx, the diagnosis is typically a combination of noninvasive diagnostic imaging, serology, and clinical presentation. The patient is a young male with no risk factors for premature coronary artery disease and his clinical presentation is more consistent with a viral myopericarditis, with low concern for coronary ischemia, and thus would be a good candidate for Cardiac MRI. CT Coronary Angiography would not be the most appropriate test given low concern for coronary artery disease and a clinical picture highly consistent with viral myocarditis. Echocardiography would definitely provide information about cardiac function, but Cardiac MRI is a superior test for this scenario because it can provide ancillary information about findings suggestive of myocarditis such as myocardial edema and gadolinium enhancement. Transesophageal echocardiography as a test is rarely indicated in myocarditis. Invasive ventriculography can be performed with a left heart catheterization but should be reserved for when left ventricular function is unknown, and there is an indication for invasive catheterization. Thus, cardiac MRI would be the best first choice.
A 65-year-old male presents to the Emergency Department with cough, malaise, and fevers to 39°C. His past medical history is notable for hypertension, diabetes, and a drug-eluting stent placed into his distal right coronary artery 5 years before angina. He has no anginal symptoms at rest. He takes aspirin, atorvastatin, metoprolol, lisinopril, and metformin. Testing with viral panel in the Emergency Department resulted in positive PCR for Influenza A. Electrocardiogram shows:
and a Troponin-T is <0.01 ng/mL. Over the course of the first 2 hours after presentation, he becomes increasingly hypoxemic, ultimately transferred to the ICU after intubation. His chest radiograph before intubation shows bilateral infiltrates. Oxygenation slowly improves over the next 12 hours. The morning after admission, he is noted to have a short run of wide complex tachycardia. Electrocardiogram shows new left bundle branch block (LBBB). He then continues to have frequent regular wide complex tachycardias, causing hemodynamic instability. Troponin-T now increases to 0.48 ng/mL.
Which of the following is the BEST next step in managing his cardiac status?
Correct Answer: A
The recurrent tachyarrhythmias that appear to be ventricular in origin in association with hemodynamic instability and rising troponin-T is concerning for active myocardial ischemia. This supports performing cardiac catheterization for diagnosis and potential reperfusion. In the absence of hemodynamic instability, a more conservative approach with echocardiogram and serial troponin-T would be a reasonable alternative. However, LBBB would cause paradoxical septal motion on echocardiography, which may confound assessment of focal wall motion abnormalities as part of the ischemic evaluation.
Though prior guidelines associate a new LBBB with ischemia, recent studies have questioned this assumption. Studies show that a new LBBB is rarely caused by acute transmural ischemia. Thus, the 2013 ST elevation myocardial infarction guidelines urge a more holistic assessment based on cardiac biomarkers, ECG criteria for myocardial infarction, and clinical scenario.
Though cardiac MRI is being evaluated as an alternate diagnostic modality for ischemia, it currently has no role in a hemodynamically unstable patient. A CT Pulmonary Angiogram would be useful if pulmonary embolism was being considered but is unlikely based on this patient’s clinical presentation.
A 68-year-old male with a past medical history of hypertension arrives at the Emergency Department with crushing chest pain. The pain started 1 hour ago and is substernal with radiation to his left shoulder. He is mildly diaphoretic and dyspneic. Vital signs on presentation are notable for:
His initial ECG is shown in the figure below:
Which of the following is the next BEST step to evaluate the extent of cardiac damage in this patient?
Correct Answer: D
This patient has ST segment depressions in the anteroseptal leads (V2- V4), and early R wave progression. The ST segment changes may be interpreted as anterior ischemia in the context of a non-ST segment elevation myocardial infarction, posterior STEMI is an important differential. The early R wave progression here indicates the evolution of Q waves in the posterior wall of the heart. Posterior MI accompanies ∼15%-20% of STEMIs, most commonly inferior or lateral STEMI due to perfusion of these territories and the posterior territory usually by the right coronary artery. The next most important test that can be done at bedside is to better characterize this is posterior ECG leads (V7-V9). The posterior MI leads are located in the same horizontal plane as V6, located at the posterior axillary line (V7) and paraspinal (V9), with V8 in between. If posterior leads confirm ST segment elevation, noting that the AHA/ACC guideline requires only 0.5 mm of ST segment elevation in these posterior leads, then the patient should be triaged for emergent coronary angiography.
Ultimately troponins and CK-MB are important in characterizing myocardial damage and impacting treatment and prognostication, but the first step should be to exclude a STEMI in a patient with this pattern on ECG. A right-sided ECG would be important in a patient presenting with an inferior MI to evaluate for RV infarction.
A 75-year-old male is brought to the Emergency Department with severe hypotension. He has a past medical history of heart failure with reduced ejection fraction (last EF 24%) and has not been compliant with his diuretics or diet. He has been admitted multiple times in the past year for heart failure exacerbations. On arrival to the Emergency Department, he is cool and minimally responsive with an initial blood bilateral pressure of 70/40 mm Hg. He is started on dobutamine and norepinephrine. On arrival to the ICU, the patient has a right radial arterial line placed without complication. The monitor reports a blood pressure of 65/55 mm Hg. The blood pressure is immediately rechecked manually, and a reading of 80/40 mm Hg is obtained.
Which of the following is the MOST likely reason for this discrepancy?
Arterial lines are useful to receive quick and real-time information about a patient’s hemodynamics. An arterial line has a catheter (inserted into the patient) that transmits the pressure wave to the fluid-filled tubes of the monitoring system. The tubing system carries the impulse of the pressure wave to the transducer, which converts the mechanical pressure signal to an electrical signal that is then presented on the monitor as a waveform. There are three steps in the calibration of an arterial pressure line:
If the arterial line system is not primed, an air bubble is introduced into what should be a fluid-filled tubing system. Air dampens pressure signals more than fluid does, so if an air bubble is introduced into the system, the waveform amplitude reflects serious dampening and reads systolic pressures as lower than actual and diastolic pressures higher than actual.
Underdamping can be caused by aortic regurgitation or hyperdynamic states such as sepsis (that would cause a widened pulse pressure). Disappearance of the diastolic waveform can be seen in patients with significant peripheral vascular disease.
A 70-year-old male with past medical history of mild-moderate mitral regurgitation and moderate-severe tricuspid regurgitation, COPD, and secondary pulmonary hypertension presents to the Emergency Department with a fever and new cough. Vitals on presentation are notable for a blood pressure of 80/43, temperature of 38.7°C, and oxygen saturation of 80% on room air, which improves modestly with 6 L oxygen by nasal cannula. Chest radiograph shows multifocal airspace opacities suggestive of pneumonia, but not pulmonary edema. He is transferred to the ICU for intubation. Examination is also notable for cool extremities with +1 symmetric lower extremity edema. In determining whether to administer fluids to this patient to augment his mean arterial pressure, which of the following techniques would be LEAST helpful?
Measures of fluid responsiveness can be separated into static and dynamic measures. The static measures include: CVP, pulmonary capillary wedge pressure, and clinical static endpoints (heart rate, blood pressure, etc). Dynamic measures include: pulse pressure variation, stroke volume variation, IVC collapsibility, and response to passive leg raise. Each of these has their own strengths and weaknesses, with dynamic measures generally thought to perform better than static measures. The 2016 surviving sepsis guidelines recommend using dynamic indices of volume responsiveness to guide volume resuscitation in sepsis.
The patient in the question has pulmonary hypertension and significant tricuspid regurgitation, which would confound interpretation of CVP measurements, if the CVP were to be used as a proxy for RV preload. However in patients with RV failure or severe TR, the CVP is falsely elevated and does not give an accurate representation of preload. The other measures of fluid status such as pulmonary artery wedge pressure (measure through a pulmonary artery catheter) measures left ventricular preload and thus a better representation of systemic preload than CVP. Dynamic indices such as pulse pressure variation, stroke volume variation, and passive leg raise have been shown to be superior measures for determining volume responsiveness.
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