For the patient with acute myocardial infarction (AMI) pressing priorities exist. Symptoms must be ameliorated, lethal arrhythmias identified and treated, arteries opened, and complications identified and managed. In many cases, little is needed beyond a targeted history and physical examination, 12-lead electrocardiogram (ECG), and simple, rapid blood work with prompt thrombolysis or emergency coronary arteriography and balloon angioplasty with or without stenting. In such straightforward cases, point-of-care echocardiography will prove interesting and perhaps helpful if potential complications are identified early. Such study, however, should never delay needed efforts at reperfusion. In other cases, the history and physical examination may be confusing, or ECG and enzymatic data may be conflicting, misleading, or delayed. These situations include (1) typical symptoms but normal or equivocal laboratory studies, (2) atypical symptoms with equivocal or abnormal laboratory studies, (3) pacemaker therapy, (4) left bundle branch block (LBBB) on ECG, (5) presence of new systolic murmur, (6) shock including right ventricular myocardial infarction, (7) late clinical presentation including post-myocardial infarction (MI) pericarditis, (8) large, non-Q-wave MI, (9) true posterior MI, and (10) suspected LV thrombus. In these instances, point-of-care ultrasonography is not only beneficial but also it may be critical for improving the understanding of the patient’s condition and selecting appropriate treatment.

For point-of-care echocardiography to prove helpful in the acute MI setting, a simple, rapidly activated and portable machine must be present in the proximate clinical area. This machine must provide good-quality two-dimensional and colored Doppler images on a wide variety of challenging patients (chronic obstructive pulmonary disease, obesity). Handheld machines, which are small enough to fit in a laboratory coat pocket, are now available at reasonable cost. In most situations, a full, formal follow-up echocardiogram should be obtained with results correlated to the point-of-care echocardiography findings. Point-of-care operators require training in theory and hands-on techniques plus proctored imaging and interpretation experience. These providers will need to work closely with institutional credentialing bodies to ensure that standards of initial training, ongoing training, and quality assurance are identified and met.

The three standard windows should be interrogated in each patient with and without color-flow Doppler (Figure 13-1A,B). Apical views should be examined first because the two-chamber, four-chamber, and five-chamber views are often readily obtained and identify all left ventricular myocardial segments in addition to the right ventricle (Figure 13-1A). Aortic, mitral, and tricuspid valves are easily identified. Color-flow interrogation in the apical views readily identifies ventricular septal defects and aortic, mitral, and tricuspid insufficiencies. Left parasternal short-axis views should be obtained next with expected good visualization of the mid-left ventricle and left ventricle at base plus aortic and mitral valves en face (Figure 13-1B). The pulmonic valve is often best seen as the aortic valve is brought into view and the transducer rotated slightly to include the right ventricular outflow tract and main pulmonary artery. The left parasternal long-axis views usually miss the left ventricular apex and may provide suboptimal visualization of the inferior and posterior walls even with the gain turned up. The aortic and mitral valves are usually well seen and color-flow Doppler provides good visualization of aortic and mitral insufficiencies. Although difficult to obtain in obese patients and in patients with severe chest pain or congestive heart failure, subcostal views prove helpful in visualizing left and right ventricular endocardium in addition to left atrium, right atrium, and aortic, mitral, and tricuspid valves. Sometimes, adequate visualization of the left ventricular apex will only be available in these views. Having the acutely ill, patient bend at the knees will often help in obtaining subcostal views. Sometimes the images are only obtainable after initial medical therapy with oxygen, nitrates, morphine, and diuretics.

During each study, every reasonable effort should be made to identify each major myocardial segment, right ventricular free wall, left atrium, right atrium, aortic, mitral, pulmonic, and tricuspid valves with and without color interrogation. Aortic root, ascending aorta, transverse aorta, and descending aorta should be identified. Pericardial effusion, ventricular septal defect, and left ventricular thrombus should be sought. Structures not adequately visualized cannot be described. If the endocardium is not seen, a wall motion abnormality cannot be identified. After the study, findings must be recorded, even when incomplete or limited, for later correlation and quality assurance. Never make bad decisions based on bad images. The point-of-care echocardiographer must always be ready to obtain assistance from another echocardiographer who may be able to acquire better images, or obtain help from another technology such as cardiac computerized tomography, transesophageal echocardiography, or cardiac catheterization.

Patients may present acutely with typical chest discomfort with symptom onset less than 1 h. The initial ECG may show only peaked T waves or anterior ST-segment depressions. Initial bedside cardiac enzymes may well be negative. With continued ischemia more ST-segment elevations may be seen on subsequent ECGs prompting thrombolysis or emergent catheter-directed intervention. Continued symptoms and positive enzymes might similarly prompt a trip to the catheterization laboratory even without classic ST-segment elevations. During the time between presentation and decision, muscle loss will continue.

When initial diagnostic confusion and uncertainty might lead to costly delays, immediate bedside echocardiography can result in diagnostic clarity and timely reperfusion. In patients presenting very early with acute MI, enzymes will be normal and ECG may show only peaked (hyper acute) T waves. A true posterior MI may show only anterior ST-segment depressions, mirror images of ST-segment elevations. These changes may be unrecognized, subtle, or, in the case of peaked T waves, due to hyperkalemia. Occasionally, similar T waves may occur in young, healthy athletes with or without symptoms. Waiting for ECG evolution or abnormal cardiac enzymes can lead to delay with unnecessary myocardial muscle loss. Bedside echocardiography demonstrating clear segmental wall motion abnormality will prompt earlier decision, treatment, and myocardial salvage.

A minority of patients with acute ischemia lack typical chest discomfort. Atypical presentations include shortness of breath, diaphoresis, nausea, vomiting, abdominal pain, syncope, profound weakness, and feeling of doom. Diabetic and postoperative patients are often asymptomatic or nearly so. Appropriately, emergency department physicians, intensive care physicians, and internal medicine and cardiology consultants cast a broad diagnostic net in these situations. Minor cardiac enzyme abnormalities and nonspecific ECG changes frequently result. Should aggressive treatment await further testing hours down the line? Should the risks of intervention be undertaken in high comorbidity patients without better information? For example, no one likes to take a fresh postoperative patient to the catheterization laboratory for urgent angioplasty with or without stent placement. Immediate echocardiography may show little or no segmental wall motion abnormality. Such a patient should do well with a conservative approach. If a large segmental wall motion abnormality were found, the more aggressive invasive approach might well be worth an increased risk of bleeding in an effort to achieve significant myocardial salvage. Even if catheter-directed intervention did not follow, a large defect might prompt intensive care unit monitoring and more intensive medical therapy.

Ventricular pacing may certainly mask an acute transmural MI. In the presence of an acute MI, echocardiography will often demonstrate a new segmental wall motion abnormality over and above the expected LBBB contraction timing abnormality seen with right ventricular (RV) pacing (Figure 13-2). A nontransmural event may or may not lead to a noticeable segmental wall motion abnormality. Following a fresh pacemaker lead implantation, a lead tip perforation may cause pericardial irritation with or without a pericardial effusion. Rarely, cardiac tamponade may result. Imaging may avert inappropriate anticoagulation with possible dire consequences, and lead, instead, to pericardiocentesis when cardiac tamponade is present.