Chapter 6. Cardiac

Echocardiography is the gold standard for the diagnosis of many cardiac abnormalities. Point-of-care echocardiography (or focused cardiac ultrasound), performed and interpreted by clinicians, was described 25 years ago.1–3 Since then, there has been a significant amount of accumulated data to demonstrate that this practice changes management and improves patient care.4–73 Clinician-performed echocardiography is now a well-accepted part of the practice of emergency medicine.43,74,75 In addition, clinicians who manage critically ill or injured patients in other clinical settings are adopting the practice of focused cardiac ultrasound.76–115

Focused cardiac ultrasound is not meant to replace comprehensive echocardiography; it is a completely different paradigm in which a goal-directed examination is meant to answer specific clinical questions, not to detect all possible cardiac pathology. Some clinicians may use cardiac ultrasound to answer just one clinical question and others may use it for a wide variety of applications. Regardless, most focused cardiac ultrasound applications are relatively straightforward to learn because they rely on simple two-dimensional (2D) imaging and pattern recognition.116

Focused transthoracic echocardiography is an ideal diagnostic tool for detecting life-threatening cardiac conditions in the ED. Some of the information obtained from focused cardiac ultrasound could be obtained by invasive monitoring techniques, but it is not practical to use invasive techniques on all patients with potentially life-threatening conditions. In addition, placement of invasive monitoring devices is time consuming and is associated with complications.

Without bedside echocardiography, clinicians are left to manage critically ill patients with only indirect information about cardiac structure and function. “Classic” physical examination findings are often absent and unreliable for making critical diagnoses. Electrocardiograms (ECGs) are very helpful in patients with certain cardiac problems, but the majority of critically ill patients have nonspecific ECG findings. Chest radiographs provide very limited information about cardiac structure and function.

In cardiac arrest with pulseless electrical activity (PEA), it is critical to determine whether the patient has true electromechanical dissociation (EMD) with cardiac standstill or pseudo-EMD with mechanical cardiac contractions too weak to generate a palpable blood pressure.117 Many patients with PEA have severe hypovolemia, while others have cardiac tamponade, massive pulmonary embolism (PE), or severe left ventricular dysfunction. All of these conditions can be detected with bedside transthoracic echocardiography. Echocardiography can be performed serially during a critical resuscitation as long as the examination itself does not interfere with resuscitative efforts.

Point-of-care cardiac ultrasound is also useful in stable patients with a wide variety of presentations. Pericardial effusions often cause nonspecific or minimal symptoms until tamponade develops. Focused echocardiography is the most efficient method to evaluate for a “silent” pericardial effusion since it is not reasonable to order a comprehensive echocardiographic examination on every patient with vague complaints who may have a pericardial effusion. Also, about 6% of all patients over 45 years of age have “silent” heart failure.118,119 Many patients also have “silent” valvular disease and may benefit from focused echocardiography, even if the valves are not fully evaluated and the only information gained is the presence or absence of gross chamber enlargement. Transesophageal echocardiography (TEE) is used widely in the perioperative and intensive care settings and has the potential to be very useful in the hands of emergency physicians.7

Any patient at risk of significant CV compromise is a candidate for a focused bedside echocardiographic examination. Patients with significant disease have widely varying presentations, from cardiac arrest to vague symptoms of dizziness, shortness of breath, or chest discomfort.6,40 The challenge is to determine which echocardiographic findings can be readily recognized by noncardiologists with minimal training and which patients need comprehensive echocardiography.

Primary indications for focused cardiac ultrasound include:

• Cardiac arrest
• Pericardial effusion and tamponade
• Massive pulmonary embolism
• Left ventricular structure and function
• Volume status and fluid responsiveness
• Unexplained hypotension
• Guidance of emergency cardiac pacing

Other indications for focused cardiac ultrasound include:

• Valvular abnormalities
• Proximal aortic dissection
• Myocardial ischemia and infarction

Cardiac Arrest

Bedside echocardiography is invaluable for directing management in cardiac arrest or near cardiac arrest states. Prior to the 1980s, all patients who had an organized electrical rhythm but no pulse were thought to have EMD. In the mid-1980s, using arterial catheters and echocardiography, physicians discovered that many patients with apparent EMD have mechanical contractions that are too weak to produce a blood pressure detectable by palpation.1,2,10,117,120

A 1988 study described two very different categories of EMD, those with “true” EMD and those with mechanical cardiac contractions. It observed that those with “true” EMD, or cardiac standstill, have a dismal prognosis, similar to the prognosis for asystole.2 Several studies reported that more than half of patients with PEA have mechanical cardiac contractions.10,13,63,121 In addition, multiple studies reported that patients initially thought to be in asystole may have cardiac contractions.13,63,122

Studies have confirmed that palpation of pulses is an unreliable means of assessing cardiac function and blood pressure. One study questioned whether carotid, femoral, or radial pulses correlated with certain blood pressure measurements.123 They attempted to palpate pulses in 20 hypotensive patients who had arterial lines and invasive blood pressure measurement already established. They found that as systolic blood pressure declined the radial pulse always disappeared before the femoral pulse, which always disappeared before the carotid pulse. Surprisingly, the absence of pulses from a specific location did not correlate with an absolute blood pressure but was widely variable; for instance, several patients had palpable carotid pulses with a measured systolic blood pressure between 30 and 60 mm Hg. More worrisome was the finding that about 10% of these patients had no palpable carotid pulse with measured systolic blood pressures between 50 and 80 mm Hg.123

Since carotid pulses have been shown to be an unreliable means for determining true cardiac arrest, basic life support guidelines put forth by the American Heart Association have de-emphasized carotid pulse checks for both lay rescuers and health-care providers.124 One study found that health-care providers are often inaccurate and unsure of themselves when doing carotid pulse checks during CPR.121 Bedside echocardiography allows clinicians to directly visualize the heart and determine the presence and quality of mechanical cardiac function during a cardiac arrest. If a carotid pulse is absent but echocardiography shows reasonable mechanical cardiac function, then clinicians should proceed with aggressive resuscitation.

Several studies have examined whether bedside echocardiography in PEA can predict the outcome of cardiac arrest resuscitation. A 2001 study reported that 56% of patients presenting to two community hospitals with PEA had cardiac contractions on bedside echocardiography; 26% of those with contractions and 4% (one patient) with cardiac standstill survived to hospital admission.63 A 2012 study reported that 24% of cardiac arrest patients had cardiac movement; 40% of those with contractions and 3% (one patient) with cardiac standstill survived to hospital admission.125 In a multicenter trial from four academic medical centers, 32% of patients with PEA had mechanical contractions; 73% of those with mechanical contractions had return of spontaneous circulation and no patient with cardiac standstill had return of spontaneous circulation.62 A 2010 study showed that 35% of those initially thought to have asystole and 58% of those with PEA had coordinated cardiac motion. They also reported that early echocardiography altered management in 78% of patients with cardiac arrest or shock.13

In current practice, many emergency physicians use echocardiography to confirm cardiac standstill before terminating resuscitation in all cardiac arrests. It may be reasonable to consider terminating resuscitative efforts in patients with PEA and cardiac standstill (true EMD). However, it is important to understand that some studies have shown that PEA with cardiac standstill is uniformly fatal, but others show a 3–8% survival to hospital admission after initial cardiac standstill.8,13,62,63,125 This discrepancy is probably due to varying definitions of the term “cardiac standstill.”

Beyond predicting the outcome of resuscitation, echocardiography is essential to rapidly identifying the cause of the cardiac arrest. Pulseless patients with nonshockable rhythms often have reversible conditions and can be treated successfully if those conditions are identified early.117 The most common causes of PEA are listed in Table 6-1.117 Hypovolemia, cardiac tamponade, massive PE, and massive myocardial infarction can be detected by bedside echocardiography so that early aggressive management of these abnormalities can be instituted.13,38,125–128

Cardiac ultrasound should be used in an advanced life support (ALS) conformed manner, so that ultrasound does not interrupt or delay standard ALS care.13,14,129,130 This is accomplished by performing cardiac ultrasound only during scheduled pulse checks according to the ALS protocol.14

The first question to answer using bedside echocardiography is whether the etiology of the arrest is likely to be cardiac or noncardiac. Severe left ventricular dysfunction will be apparent. Some investigators have reported using a similar approach to determine whether hypotension had a cardiac or noncardiac etiology. The authors compared 2D echocardiography with hemodynamic measurements from pulmonary artery catheters and found that in 86% of cases echocardiography correctly determined whether the etiology of shock was cardiac or noncardiac.131 In addition, studies have shown that emergency physicians can accurately estimate left ventricular function, especially when left ventricular dysfunction is severe.44,52,58

One prospective study used cardiac ultrasound in an ALS-conforming manner to identify patients with “pseudo-PEA” (cardiac contractions but no palpable pulses).130 When cardiac contractions were noted, they extended the 10-second pulse check to 25 seconds and immediately administered 20 units of vasopressin, and then rechecked for pulses. Fifteen of 16 (94%) of these patients had return of spontaneous circulation and 8 patients (50%) had good neurologic outcome.

Patients in cardiac arrest with PEA as a result of severe hypovolemia will have a small, empty-appearing heart on bedside echocardiography.126 Both the right and left ventricles will be poorly filled and the right ventricle will be almost completely collapsed. The left ventricle will usually be vigorous. The inferior vena cava (IVC) will have a small diameter and its lumen will disappear completely during inspiration (or expiration when positive pressure ventilation is being used). These findings on bedside echocardiography should prompt the clinician to aggressively replace volume and consider the etiology of hypovolemia.

One of the most straightforward applications of bedside echocardiography during cardiac arrest is evaluating for a pericardial effusion.2,56,57 A pericardial effusion presents as an anechoic stripe surrounding the heart and should be obvious if it is large enough to cause cardiac tamponade. This finding should prompt the clinician to perform an immediate pericardiocentesis using ultrasound guidance (See Chapter 8, “Critical Care” and Chapter 22 “Additional Ultrasound-Guided Procedures,”). Pericardiocentesis can be lifesaving and the removal of just a small amount of fluid may result in significant improvement in cardiac output.1,2,41,127

Massive PE is responsible for about 10% of cardiac arrests in cases where a primary cardiac etiology is clinically suspected.132,133 The routine use of bedside echocardiography in cardiac arrest may allow immediate detection of massive PE, even in cases where the diagnosis is not clinically suspected.26,32,38,39,134,135 It is important to immediately recognize that PE is the cause of a cardiac arrest because early thrombolytic therapy has been shown to significantly improve the chance of return of spontaneous circulation. A review of 60 cases of cardiac arrest caused by massive PE found that 81% of patients who received early thrombolytic therapy had return of spontaneous circulation compared with 43% for those who did not receive the therapy.132

There is some evidence that TEE may be an attractive alternative to the transthoracic approach for patients in cardiac arrest. Image quality is better with transducer placement in the esophagus due to its proximity to the heart and lack of artifacts caused by interpositioned lung or bone tissue. It is not affected by body habitus or subcutaneous air. Perhaps the biggest advantage is the ability to minimize the interruption of chest compressions for transthoracic imaging. The TEE transducer may be left in place during the entire resuscitation and usually does not require changes in position, allowing the entire team to continuously view the heart. In addition, it is electrically isolated, so it can even be left in place during defibrillation.

A 2008 publication reviewed six cases where TEE offered distinct advantages over transthoracic echo, including detection of occult pathology in two patients who had aortic dissection and PE.7 A 2009 study showed that TEE can be used to evaluate the effect of chest compressions and reported inadvertent compression of the aortic root or left ventricular outflow tract (LVOT) resulting in a 19–83% incidence of outflow obstruction during chest compressions.136 TEE is generally considered a very safe imaging modality and the incidence of esophageal injury is extremely low (0.03%).137 The additional equipment costs, learning curve, and maintenance issues associated with this technique may limit generalized use of TEE in point-of-care sonography.

Pericardial Effusion and Tamponade

In 1992, Plummer reported 100% sensitivity for recognizing pericardial effusion in the first 6 years after his group of emergency physicians began screening penetrating trauma patients with bedside echocardiography. More importantly, the use of bedside echocardiography significantly reduced the time to diagnosis and disposition to the operating room from 42 minutes to 15 minutes, while patient survival improved from 57% to 100%.55 Bedside focused echocardiography is now the standard of care for patients with potential penetrating cardiac injuries (Figure 6-1).108,138,139

Patients with nontraumatic pericardial effusions are more difficult to identify because clinical signs and symptoms are inconsistent. Most patients with clinically significant pericardial effusions have nonspecific symptoms such as tachycardia, dyspnea, chest pain, cough, or fatigue.140–144 Since cardiac tamponade can develop rapidly, even in those with chronic pericardial effusion, it is prudent to make the diagnosis as early as possible. Table 6-2 lists the disease processes that place patients at risk of pericardial effusion.142,145 Effusions associated with neoplastic disease or bacterial, fungal, or HIV infections have a higher risk of progressing to tamponade.145 In addition, patients who have had recent catheter-based cardiac procedures, like coronary angiography or pacemaker/defibrillator placement, or cardiothoracic surgery, are at increased risk of a pericardial effusion that progresses to tamponade.143,146

Any patient with a pericardial effusion is at risk of developing cardiac tamponade, which is a life-threatening condition that occurs when a pericardial effusion causes significant compression of the heart leading to a decrease in cardiac output. When a pericardial effusion develops acutely, tamponade can occur with as little as 150 mL of fluid. Because the parietal pericardium can stretch over time, a chronic effusion can have a volume of >1000 mL without causing tamponade. The rate of pericardial fluid accumulation relative to pericardial stretch is the critical factor (Figure 6-2). The steep rise in the pericardial pressure–volume curve makes tamponade a “last-drop” phenomenon; the last few milliliters of fluid accumulation produce critical cardiac compression and the first milliliters of drainage produce the largest relative decompression.142,145 Cardiac tamponade can present with nonspecific signs and symptoms and rapidly progress to hypotension, PEA, and death if not rapidly diagnosed and treated.140–144,147 Echocardiography is the best imaging modality to evaluate for pericardial effusion or tamponade.74,144,146,148 In addition, ultrasound-guided pericardiocentesis is the gold standard for percutaneous drainage of significant pericardial effusions (see Chapter 8, “Critical Care” and Chapter 22, “Additional Ultrasound-Guided Procedures”).144,146,148

Pericardial effusions are often asymptomatic or associated with nonspecific symptoms. One study evaluated bedside echocardiography on 103 patients with unexplained dyspnea and found that 14 had pericardial effusions. Four had large effusions requiring pericardiocentesis and three had moderate-sized effusions that were treated conservatively. The authors recommended that ED patients with unexplained dyspnea should be evaluated for pericardial effusion.6 Another study evaluated the accuracy of bedside echocardiography performed by emergency physicians to detect pericardial effusions. High-risk symptoms included unexplained hypotension or dyspnea, congestive heart failure, cancer, uremia, lupus, or pericarditis. They found 103 pericardial effusions in this high-risk population and determined that bedside echocardiography by emergency physicians was 97.5% accurate for making this diagnosis.40

Historically, the diagnosis of tamponade is a clinical diagnosis based on symptoms and physical exam findings.142 However, symptoms and physical exam findings of cardiac tamponade are variable.149 Pulsus paradoxus may be the most useful sign, but is not perfectly accurate for making the diagnosis. Pulsus paradoxus may be absent in patients with tamponade who also have left ventricular dysfunction and intubated patients who are receiving positive pressure ventilation.150 Patients with loculated pericardial effusions may develop regional tamponade of the left ventricle. This tends to occur following cardiac surgery, does not result in pulsus paradoxus, and may be missed by point-of-care ultrasound if multiple cardiac views are not assessed.23 In addition, pulsus paradoxus may be present in patients with emphysema in the absence of tamponade.150 Therefore, physical exam findings of tamponade are often misleading and may be inadequate for making decisions regarding intervention. Both physical exam and echocardiographic signs need to be considered when making the diagnosis of tamponade (Table 6-3).

Most nonhemorrhagic pericardial effusions that cause tamponade are moderate to large (300–600 mL) in size.142 Therefore, an indication for emergent pericardiocentesis is the finding of a moderate or large effusion in a patient with clinical signs of tamponade. Large pericardial effusions surround the entire heart while small effusions may collect first around the more dependent, mobile ventricles.57 Effusions can be categorized by the maximal width of the anechoic pericardial stripe. A stripe <10 mm is small, 10–15 mm is moderate, and >15 mm is large.6 These are gross measurements and do not correlate perfectly to the volume of the effusion. Also, hemorrhagic effusions can occur outside the setting of trauma and tend to accumulate rapidly and cause tamponade even when they are small.

Massive Pulmonary Embolism

It is estimated that there are 300,000–600,000 cases of deep vein thrombosis (DVT) or PE each year in the United States.151 In 25% of patients with DVT or PE there are no symptoms prior to cardiac arrest, and PE accounts for 60,000–100,000 deaths per year.152 Patients who are hemodynamically stable at the time of PE diagnosis have a good prognosis, but those with a massive PE with hemodynamic compromise have a mortality rate of 25–50%.153 Patients who present in extremis require rapid intervention since 70% of patients who die from PE do so within the first hour. Early thrombolytic therapy or embolectomy is required and rapid treatment often precludes obtaining time-consuming imaging studies.154–161

Bedside echocardiography can be used to rapidly confirm or refute the diagnosis of massive PE and shorten the time between patient presentation and treatment.26,32,39,135 The echocardiographic findings in massive PE are not subtle and include massive right ventricular dilatation and right-sided heart failure with a small, vigorously contracting left ventricle (Figure 6-3).38 In some cases, thrombus can actually be seen in the right atrium or ventricle. Point-of-care ultrasound can also help point to an alternative diagnoses in patients with symptoms that mimic PE, such as cardiac tamponade, pneumothorax, or left ventricular dysfunction.74 It is important to understand that patients may have other underlying diseases that cause chronic right-sided heart strain, thus making the diagnosis of acute cor pulmonale in these patients difficult and unreliable.162

In patients with a high pretest probability of PE, ultrasound findings of overt right ventricular failure clinch the diagnosis and put the patient into a high-risk group that may benefit from thrombolytic therapy or surgical embolectomy.163,164 Patients with massive PE often present with syncope, hypotension, cardiogenic shock, and cardiac arrest. The 2008 American College of Chest Physicians (ACCP) evidence-based clinical practice guidelines recommend fibrinolysis (Grade 1B evidence) for patients with acute PE and hemodynamic compromise.165 They also warn that delaying fibrinolytic therapy may result in irreversible cardiogenic shock.165 Investigators who performed a randomized trial of thrombolytic therapy for massive PE stopped their study early due to ethical concerns after enrolling only eight patients. Four patients who received streptokinase and heparin lived and did not have significant pulmonary hypertension on 2-year follow-up. All four patients treated with heparin alone died within 3 hours after arrival to the ED.166

The management of hemodynamically stable PE with echocardiographic findings of severe right ventricular failure (submassive PE) is controversial.167 Although the ACCP guidelines recommend against throm-bolytic therapy in patients with submassive PE, they note that thrombolytics are an option (Grade 2B evidence) for normotensive patients with an acute PE and right ventricular dysfunction who have a low risk of bleeding. The key point is that patients with echocardiographic findings of overt right heart failure have a massive clot burden and are at very high risk of death, regardless of whether they are hypotensive. A prospective study of 200 patients with submassive PE found that those treated with thrombolytic therapy had a much lower incidence of severe pulmonary hypertension 6 months after treatment.

There is good evidence that surgical embolectomy in patients with massive and submassive PE reduces mortality.163,168–171 The drawback of surgical embolectomy is that it requires mobilization of significant resources and is not an option at most institutions. If surgical embolectomy is an option, point-of-care cardiac ultrasound is important for making a rapid diagnosis, so that resources can be quickly mobilized before the patient develops irreversible heart failure.

The use of bedside echocardiography to diagnose massive PE should not be confused with using echocardiography to evaluate stable patients suspected of having PE. There is a wealth of data demonstrating that echocardiography has poor accuracy when used to rule out PE in stable patients without severe symptoms or hemodynamic compromise.172,173

Assessment of Left Ventricular Structure and Function

Echocardiography is the preferred first-line test for patients with symptoms or signs consistent with left ventricular dysfunction.174 Patients who present with nonspecific complaints may have unexpected left ventricular failure. More than half of patients with moderate-to-severe diastolic or systolic dysfunction have never been diagnosed with heart failure.119 Patients with moderate-to-severe left ventricular dysfunction are at higher risk of complications regardless of their presentation.119,175 In addition, when patients present with cardiogenic shock both short- and long-term mortality correlate with the degree of initial left ventricular systolic dysfunction and the degree of mitral regurgitation.176

Simple visual estimation of left ventricular ejection fraction is a reliable method of determining left ventricular systolic function.177–179 Several studies have demonstrated that emergency physicians can use visual estimation to accurately assess left ventricular ejection fraction, even with as little as 3 hours of training.44,52,73,90,101,180–182 It has been suggested that bedside echocardiography could be used to differentiate patients with primary pump failure from those with other potential causes of hypotension.92

One study showed that emergency physicians can reliably use qualitative visual estimates to assess left ventricular systolic function in hypotensive ED patients.73 They compared their visual estimates of left ventricular ejection fraction to measurement of fractional shortening, which is known to be a reliable method for assessment of left ventricular systolic function, and found good agreement. They also showed that their fractional shortening measurements and their visual estimates of systolic function were reproducible on serial exams.

In addition to visual estimation, there are several techniques that can be used to obtain quantitative measurements of left ventricle function. E-point septal separation (EPSS) and fractional shortening are simple measurements that can be obtained quickly. Measurement of left ventricular volumes by the biplane method of discs or calculation of stroke volume and cardiac output by measuring Doppler flow through the LVOT are more complex techniques and require advanced training.

EPSS is a simple and rapid measurement that reliably estimates left ventricular function (Figure 6-4).67,183–185 A 2011 study showed that emergency physicians with limited echocardiography experience could obtain measurements of EPSS in acutely dyspneic patients.67 These measurements correlated closely with visual estimates of left ventricular ejection fraction by clinicians with extensive echocardiography experience. In general, EPSS >7 mm indicates left ventricular dysfunction, and EPSS >13 mm indicates severe dysfunction.67,183,186,187 EPSS can reliably estimate left ventricular function in patients with aortic stenosis, but is usually misleading in patients with significant mitral stenosis or aortic regurgitation.184

Fractional shortening is a simple technique for assessing cardiac contractility based on one-dimensional (1D) measurements of the left ventricle during diastole and systole. Measurements of the left ventricular end-diastolic diameter (LVEDD) and end-systolic diameter (LVESD) with M-mode at the level of the papillary muscles are guided by 2D parasternal long- or short-axis images to calculate fractional shortening (FS) = (LVEDD-LVESD)LVEDD.52,73,188 Measurement of FS by emergency physicians has been shown to be reproducible and accurate compared with cardiology overreads.52,73

Fractional shortening should not be confused with ejection fraction. A normal value for fractional shortening is >25%, whereas a normal left ventricular ejection fraction is >55%.189 Also, fractional shortening <15% is consistent with severe left ventricular dysfunction and this correlates with a left ventricular ejection fraction of <30%.189 Most modern ultrasound machines can calculate left ventricular ejection fraction when fractional shortening is measured. These calculations assume that the left ventricle has a “normal” shape and symmetrical function, so this method of determining left ventricular ejection fraction may be inaccurate in patients with regional wall motion abnormalities or oddly shaped ventricles. This method can also be inaccurate if the M-mode cursor is not exactly perpendicular to the septum and posterior wall.

The optimal method to measure left ventricular ejection fraction is using the method of discs (modified Simpson's rule).189 This involves tracing the endocardial border during diastole and systole, so that the computer can calculate the change in left ventricular volume. It is most accurate if measurements are performed in two orthogonal planes (apical four-chamber and apical two-chamber views), which is known as the biplane method of discs.189 Some modern ultrasound machines can calculate the left ventricular ejection fraction from one plane (usually the apical four-chamber view), which may be more practical in the point-of-care setting.

Calculation of left ventricular ejection fraction by the method of discs will be inaccurate if true apical views are not obtained and foreshortened (oblique) views of the left ventricle are measured. Also, it is often difficult to visualize the endocardial border, even if good images are obtained. Many echocardiography labs routinely use contrast agents to improve endocardial border detection. Contrast echocardiography significantly improves the accuracy and reproducibility of measuring left ventricular ejection fraction.190,191 Contrast is especially useful in obese patients and those with lung disease.192 This has not been well studied in the setting of clinician-performed focused cardiac ultrasound, but it has been found in ICU patients that the left ventricular ejection fraction was uninterpretable on 23% of exams using standard echocardiography, 13% using harmonic echocardiography, and 0% with contrast echocardiography (Figure 6-5).191

It is important to realize that fractional shortening and left ventricular ejection fraction are measurements of left ventricular dimension variation and not measurements of stroke volume and cardiac output. Patients with significant mitral regurgitation may have a hypercontractile left ventricle but a very low cardiac output, and patients with dilated cardiomyopathy may have a good stroke volume despite a low ejection fraction. When these clinical conditions are known or suspected it may be reasonable to correlate left ventricular ejection fraction with measurements of stroke volume. Stroke volume can be measured by obtaining two variables: (1) the area of the LVOT and (2) the velocity time integral (VTI) of the flow through the aortic valve during systole. Measuring stroke volume and cardiac output is not a routine part of point-of-care ultrasound, but it is not difficult for practitioners who have learned to obtain the standard echocardiographic views.

Although significant left ventricle systolic dysfunction (left ventricular ejection fraction <30%) is usually obvious in cases of cardiogenic shock and severe heart failure, it is important to understand that cardiac function includes more than just left ventricular contractility. Left ventricular ejection fraction may not be a good indicator of cardiac output in patients with aortic stenosis, mitral regurgitation, and concentric left ventricular hypertrophy (LVH).193 Also, isolated left ventricular diastolic dysfunction is a significant cause of heart failure. Approximately 50% of patients with overt congestive heart failure have isolated left ventricular diastolic dysfunction, with normal left ventricular systolic function.119,194,195

Assessing for diastolic dysfunction usually requires Doppler measurements and was previously considered an advanced cardiac ultrasound skill. However, a 2010 study showed that emergency physicians with limited training could rapidly and accurately use pulsed Doppler to evaluate diastolic function in patients presenting with acute dyspnea.48 The investigators performed simple Doppler measurements of transmitral velocity and noted whether a restrictive filling pattern was present or absent. They found that a restrictive filling pattern was more sensitive and specific than visual estimation of reduced left ventricular ejection fraction, the Boston criteria, or N-terminal prohormone brain natriuretic peptide for identification of left ventricular heart failure.

A complete assessment of left ventricular diastolic function and filling pressures requires a combination of pulsed Doppler transmitral and tissue Doppler mitral annular measurements.194,196–199 This is not difficult to learn and may be reasonable for emergency physicians with significant ultrasound experience.45,200 Using pulsed Doppler to assess for simple indices, such as transmitral peak E velocity alone, may allow less experienced clinicians to assess for elevated filling pressures associated with diastolic heart failure.201 Also, simple M-mode measurement of left atrial emptying fraction may be a practical technique for determining diastolic dysfunction.202

Left atrial enlargement (LAE) is an important marker of left-sided heart disease and a strong predictor of congestive heart failure, hospitalization, stroke, and mortality.189,203–206 LAE is usually the result of elevated filling pressures caused by left ventricular diastolic dysfunction, but can also be caused by volume overload from valvular regurgitation and high output states like chronic anemia.189,207–210 LAE may be obvious on multiple cardiac views and can be quickly confirmed by measuring the end-systolic atrial diameter in the parasternal long-axis view. If this measurement is >4 cm or significantly larger than the proximal aortic diameter, then LAE is likely (Figure 6-6).183,189,211–219 A single-plane area can also be measured, but the optimal way to evaluate for LAE is measurement of left atrial volume using the biplane area-length method or the Simpson's method of discs.189,220

LVH is an important finding and there is a strong correlation between ultrasound measurements of left ventricular mass and subsequent coronary artery disease, sudden death, and other adverse clinical events.221–224 The sensitivity of ECG for LVH is poor and does not detect the majority of cases.221,225,226 Concentric LVH, an increase in wall thickness with normal chamber size, is usually the result of pressure overload from systemic hypertension. Eccentric hypertrophy, chamber enlargement with relatively normal wall thickness, is more common in patients with volume overload from regurgitant valvular lesions.227 Left ventricular mass can be determined by more complicated methods or by simple measurements in the parasternal long-axis view plotted on a nomogram.228,229 Normal left ventricular mass is variable depending on patient size and sex, but in general left ventricular internal chamber diameter >5.5–6.0 cm or wall thickness ≥ 12 mm, measured at the end of diastole, is suggestive of LVH (Figure 6-6).189,212,214,218,219,229

Volume Status and Fluid Responsiveness

Fluid therapy is a critical part of shock management, especially in sepsis. Aggressive early fluid resuscitation is encouraged and appropriate in most cases.230 However, not all patients benefit from aggressive fluid resuscitation and there is growing evidence that fluid overload may increase morbidity and mortality.82,110,231–236 Therefore, it is best to give fluid in a goal-directed manner using some objective parameters to help guide therapy.237,238 Point-of-care ultrasound is one of many tools that can be used to guide fluid therapy in shock because it allows a rapid noninvasive estimate of intravascular volume status and a prediction of fluid responsiveness.76,79,93,113,238–241 In addition to guiding fluid management decisions in septic shock, ultrasound assessment of intravascular volume can be used in a variety of other clinical settings, such as hemodialysis, pediatric dehydration, trauma, and heart failure.9,17,37,42,238,242–250

Estimating central venous pressure (CVP) with point-of-care ultrasound is important because historically cardiac filling pressures [CVP and pulmonary capillary wedge pressure (PCWP)] were the clinical gold standard for determining volume status and guiding fluid resuscitation. The current guidelines for the Surviving Sepsis Campaign suggest fluid resuscitation based on CVP as well as central venous oxygen saturation.251 The use of ultrasound to estimate CVP in the acute care setting, where invasive monitoring is not convenient or possible, has been one of the most important applications of point-of-care ultrasound.3,57,58,73,74

Despite the widespread use of CVP monitoring, there is significant data showing that cardiac filling pressures (CVP and PCWP) are relatively poor predictors of fluid responsiveness.107,233,252–260 Fluid responsiveness is a relatively new concept that describes a positive hemodynamic response (increase in cardiac output) to fluid therapy.76,79,93,233,237–239 The standard definition of fluid responsiveness is a >15% increase in cardiac output with a fluid bolus (500–1000 mL).240 This concept is important because not all patients who are in shock benefit from aggressive fluid therapy and several studies demonstrate that fluid overload can lead to increased morbidity and mortality.110,231,232,234–236,241 Fluid responsiveness can be predicted by measuring variations in IVC size or by assessing changes in cardiac output with the respiratory cycle or passive leg raising. Finally, an assessment of the left ventricular function and size can be used to estimate intravascular volume and the need for fluid therapy. Hyperdynamic cardiac function, small left ventricular end-diastolic area or left ventricular systolic collapse are reliable predictors of hypovolemia.79,261

Inferior Vena Cava Size and Degree of Collapse to Estimate CVP and Volume Status

The size and the magnitude of respiratory variations in the IVC correlate with CVP (Table 6-4).58,64,266,262,267–269,263,270–277 In spontaneously breathing (nonintubated) patients with a normal CVP (<10 mm Hg), the IVC collapses significantly (≥50%) with passive inspiration. IVC diameter (during expiration) is generally large (>2 cm) in patients with elevated CVP (>15 mm Hg) and small (<1 cm) in patients who are hypovolemic.47,85,248,262,263,276,278,279

The utility of using IVC indices to estimate CVP in mechanically ventilated patients is controversial.277 With mechanical ventilation, the IVC is typically less dynamic and does not exhibit significant variation with the respiratory cycle. However, a small IVC diameter (<10 mm) reliably predicts a low CVP.64,85,246,248,249,279

IVC diameter and degree of collapse correlate with volume status in the setting of hemorrhagic shock, heart failure, acute dehydration, and pre- and post-hemodialysis.37,85,86,242,246,248,249 One study found that the IVC diameter was a better predictor of recurrent shock than blood pressure, heart rate, or arterial base excess.246 Another study concluded that IVC diameter was a more accurate predictor of shock than the shock index and other commonly used noninvasive predictors of blood loss.

In the setting of hemodialysis, ultrasound assessment of the IVC has been used to help evaluate intravascular fluid volume and optimize dry weight.245,247,250,280 One study found that IVCe ≤8 mm and collapsibility ≥90% was consistent with optimal dry weight and that IVCe ≥22 mm and collapsibility ≤10% were warnings of fluid overload. Another study found that lowering the dry weight so that interdialytic IVCe was <16 mm improved volume overload and cardiac function.

In the setting of acute dyspnea, IVC measurements can be used to help support the diagnosis of heart failure. In one study of ED patients presenting with acute dyspnea, IVC collapsibility of <33% had a sensitivity of 80% (but poor specificity) for the diagnosis of acute heart failure. IVC collapsibility of <15% and an IVC diameter to aorta diameter (IVC/aorta) ratio >1.2 were both highly specific for the diagnosis of acute heart failure (both 96% specific).42

IVC/aorta ratio is also used in pediatrics because it is thought to be a more valid measurement of IVC size that is independent of patient size in smaller patients.17,36,243 The IVCe/aorta ratio may be useful for evaluating significant dehydration in children. One study found that children requiring IV hydration had a mean IVC/aorta ratio of 0.75 compared with a mean of 1.01 for controls. The IVC/aorta ratio increased to a mean of 1.09 after hydration. An IVC/aorta ratio of ≤0.8 has been found to be a relatively good indicator of significant dehydration, with a sensitivity of 86%, but a specificity of only 56%.

All IVC studies are consistent on one point: measurements of size and collapsibility are more accurate at the extremes. A small collapsing IVC is a very reliable indicator of a low CVP, and a very large IVC with no inspiratory collapse is a reliable predictor of elevated CVP. Clinicians should realize that IVC indices are only one piece of evidence and should not be used in isolation, but in combination with calculations of pretest probability and other clinical factors. Also, there are little data on following serial IVC indices, but this is a very useful technique.73 When a patient presents with hypotension, the initial treatment often involves a fluid challenge, and serial monitoring of the IVC can help clinicians evaluate changes in CVP related to fluid therapy. Serial monitoring may also help guide decisions about when to limit fluid therapy. In general, if the IVC remains flat and collapsible, more fluid can be given. When the IVC becomes large and noncollapsible, it may be wise to limit fluid or consider implementing other monitoring techniques.

There are certain clinical situations in which assessing IVC size and collapsibility may be confusing or misleading. In patients with right heart failure, the IVC may be large and poorly collapsible despite intravascular volume depletion. Therefore, it is worthwhile to reiterate that ultrasound measurement of IVC indices is not perfect and should not be used in isolation, but in combination with the clinical exam and ultrasound assessment of cardiac function.

IVC Distensibility to Predict Fluid Responsiveness in Mechanically Ventilated Patients

In mechanically ventilated patients, the changes in IVC diameter during the respiratory cycle are opposite of the changes during spontaneous breathing. The IVC does not collapse but distends during insufflation, as venous return decreases and the volume of extrathoracic venous blood increases.82 Also, variations in IVC diameter are much smaller during mechanical ventilation than with spontaneous breathing. However, if the magnitude of distention is carefully measured using M-mode ultrasound, it can be used to accurately predict fluid responsiveness.

Using IVC measurements at different times throughout the respiratory cycle, one study calculated the distensibility index, which reflects the increase in IVC diameter with mechanical insufflation. Distensibility index (dIVC) = IVCmax – IVCmin/IVCmin × 100%. The dIVC was measured before and after a 7 mL/kg volume expansion by a plasma expander. Cardiac index (CI) was also calculated from aortic Doppler measurements before and after volume expansion, and fluid responsiveness was defined as an increase in CI. The study found that dIVC >18% was an accurate predictor of fluid responsiveness (sensitivity 90%, specificity 90%) and baseline CVP was a poor predictor of fluid responsiveness. Another study calculated distensibility index as dIVC = IVCmax – IVCmin / IVCmean and found that dIVC >12% was an accurate predictor of fluid responsiveness (positive predictive value 93%, negative predictive value 92%).82

Measuring IVC distensibility to predict fluid responsiveness has several limitations. It is only reliable with mechanically ventilated patients who are perfectly synchronized to the ventilator (or paralyzed). The patient must be receiving a tidal volume of at least 8–10 mL/kg with positive pressure ventilation. Also, the patient must be in sinus rhythm and cannot have significant right-sided heart failure.

Respiratory Variation in Stroke Volume, Aortic Flow Velocity, and Arterial Peak Velocity to Predict Fluid Responsiveness in Mechanically Ventilated Patients

Intermittent positive pressure ventilation induces cyclic changes in left ventricular stroke volume, resulting in maximum stroke volume during mechanical insufflation and minimum stroke volume during exhalation.281 The magnitude of respiratory changes in stroke volume is an indicator of biventricular preload dependence and a strong predictor of fluid responsiveness.233,238,239,281 Respiratory variation in aortic flow velocity and pulse pressure accurately reflects the magnitude of stroke volume variation, so measurement of these indices can also reliably predict fluid responsiveness.233,254,256,282 Transthoracic ultrasound or TEE can be used to measure stroke volume variation and aortic flow velocity variation.83,100,283–285 In addition, point-of-care ultrasound can be used to measure peripheral artery peak velocity variation.286,287

There are some important limitations to using respiratory variations in stroke volume and aortic flow velocity to predict fluid responsiveness. The patient must be mechanically ventilated and perfectly synchronized with the ventilator (or paralyzed). They must be receiving positive pressure ventilation with a tidal volume of at least 8–10 mL/kg.288,289 Finally, analysis of respiratory changes in stroke volume is not possible in patients with cardiac arrhythmias, so patients must be in sinus rhythm.281

Changes in Stroke Volume with Passive Leg Raising for Prediction of Fluid Responsiveness in Spontaneously Breathing and Mechanically Ventilated Patients

Passive leg raising allows reliable prediction of fluid responsiveness regardless of ventilation mode or cardiac rhythm.290–293 Passive straight leg raising essentially employs an endogenous fluid challenge by effectively increasing central blood volume and filling pressures.291 Several studies show that echocardiographic measurement of stroke volume before and after passive straight leg raising enables reliable prediction of fluid responsiveness (Figure 6-7).100,102,294–296 A meta-analysis by Cavallaro et al. found that patients who had an increase in stroke volume (or cardiac output) of ≥18% with passive leg raising were fluid responsive, with a sensitivity of 89% and a sensitivity of 91%.290 In addition, point-of-care ultrasound can be used to measure changes in peripheral artery peak velocity with passive straight leg raising.297

Assessment of the Left Ventricle to Estimate Volume Status and Predict Fluid Responsiveness

Hyperdynamic left ventricular function is often seen in hypotensive patients and is generally considered an indicator of hypovolemia. Bedside cardiac ultrasound with a subjective assessment of hyperdynamic cardiac function and left ventricular systolic collapse has been found to be a better indicator of hypovolemia than CVP.261 The presence of a hyperdynamic left ventricle in patients with nontraumatic undifferentiated hypotension has been demonstrated to be highly specific for sepsis as the etiology of shock.33 A hyperdynamic left ventricle has been defined as “near or complete obliteration of the left ventricular cavity,” meaning that the endocardial surfaces of the septum and posterior wall come in close contact with each other.73 The presence of tachycardia is not a factor in making this assessment. Visual evaluation of hypercontractile left ventricular performance predicts volume responsiveness after cardiac arrest with 71–100% sensitivity.87

Left ventricular volume and end-diastolic area correlate with preload and can be assessed to help guide fluid therapy.298 Left ventricular end-diastolic area is a reliable indicator of significant hypovolemia.299–302 Subjective evaluation of left ventricular volume by assessing the size of the left ventricular cavity in the short- and long-axis views is often adequate to guide fluid therapy at the extremes of cardiac filling and function.79 Also, significant volume depletion can be recognized by assessing left ventricular volume and end-diastolic area with a single measurement of left ventricular cross-sectional area. This is measured by tracing the endocardial border at end-diastole on a short-axis view at the level of the midpapillary muscles. A left ventricular cross-sectional area value of <10 cm2 generally indicates hypovolemia (Figure 6-8A).79,189 Also, a subjective but reliable indicator of hypovolemia is the “kissing papillary muscle sign,” found to be 100% sensitive for detecting hypovolemia but only 30% specific for predicting volume responsiveness.303 It is important to note that the finding of a large left ventricular area or volume should be interpreted with caution because it does not necessarily indicate adequate filling pressure (preload) in hypotensive patients with left ventricular dysfunction.

Complete systolic obliteration of the left ventricular cross-sectional area is an accurate predictor of severe hypovolemia (Figure 6-8B).79 This is an important finding because it may be associated with dynamic left ventricular outflow obstruction. This can occur in elderly patients with concentric left ventricular hypertrophy, or in patients with apical myocardial infarction or Takotsubo cardiomyopathy. These patients are at risk for developing a dynamic outflow obstruction when they are exposed to dehydration, reduced afterload, and catecholamine stimulation.104,304–309 This can be difficult to diagnose without cardiac ultrasound because filling pressures (CVP and PAP) may be elevated despite significant hypovolemia, and patients may quickly deteriorate if pressors are increased and fluid is withheld.

Quantitative versus Qualitative Assessment of Hemodynamic and Volume Status

Although there are many measurements that can be obtained to determine volume status, filling status, and cardiac function, it is clear that clinicians can often use visual estimation to evaluate hemodynamic status. It has been found that measurements and subjective assessments were essentially equivalent when comparing serial qualitative and quantitative assessments of IVC collapsibility and left ventricular systolic function during early resuscitation in hypotensive ED patients.73

Unexplained Hypotension

One of the most useful applications of point-of-care ultrasound is the assessment of patients with unexplained hypotension. Unexplained hypotension is a common presentation in the ED and other critical care settings. The etiology of shock is often difficult to determine due to lack of patient history, confusing symptoms, and unclear physical exam findings. These patients often need early aggressive therapy, even before the diagnosis is determined. The use of point-of-care ultrasound in these patients allows clinicians to quickly assess for conditions that may have similar clinical presentations but very different management strategies.51 In this capacity, the ultrasound findings help clinicians narrow the differential diagnosis by identifying cardiac findings consistent with broad classifications of shock. In addition, other applications of point-of-care ultrasound (beyond the cardiac exam) can be used to further delineate the etiology of shock.49,74

Hypotension resulting from cardiac tamponade, massive PE, severe left ventricular dysfunction, or significant hypovolemia is usually readily apparent on bedside echocardiography.5,38,44,49,52,56–58,61,92,127,246,248 Clinicians using focused cardiac ultrasound to differentiate shock states must realize that patients may have more than one abnormality or that they may have an acute illness superimposed on a chronic cardiac condition. As with all echocardiographic findings, clinical correlation is required, but gross cardiac abnormalities are clinically relevant in the setting of hypotension.

Ultrasound detection of a pericardial effusion that is large enough to cause hypotension is relatively straight-forward.55,108,139 Ultrasound's sensitivity for detecting a clinically important pericardial effusion is nearly 100%. When a pericardial effusion is detected in the setting of hypotension, the question is whether the effusion is causing cardiac tamponade.46,149 The diagnosis of cardiac tamponade and the decision to perform pericardiocentesis are based on a combination of symptoms, physical exam findings, and ultrasound findings (see the section “Pericardial Effusion and Tamponade”).

Bedside echocardiography is essential for rapidly making the diagnosis of massive PE.26,32,39,135 Patients who are in shock due to PE, by definition, have a massive PE.159,166,171,310–313 These patients have a very high mortality and clearly benefit from rapid diagnosis and aggressive medical or surgical ther-apy.11,159,166,169,171,310–314 The echocardiographic findings are usually straightforward in cases of massive PE and include massive right ventricular dilatation and right-sided heart failure with a small, vigorously contracting left ventricle.11,38,135,315 Underlying diseases, such as emphysema, cause chronic right-sided heart strain, making the diagnosis of acute cor pulmonale difficult and unreliable (see the section “Massive Pulmonary Embolism”).162 In unclear cases, further evaluation with CT may be necessary; however, when the diagnosis of massive PE is clear, aggressive management should not be delayed.165

Cardiogenic shock is common and occurs in 5–8% of patients hospitalized for ST elevation myocardial infarction. Most patients with cardiogenic shock present with moderate or severe left ventricular systolic dysfunction.176,316,317 Isolated diastolic dysfunction can cause symptoms of heart failure, but most patients with cardiogenic shock have overt left ventricular systolic dysfunction that can be easily recognized by bedside echocardiography. Standard 2D point-of-care echocardiography can be used to quickly assess left ventricular systolic function (also see the section “Assessment of Left Ventricular Structure and Function”). Many studies have shown that simple visual estimation of left ventricular ejection fraction is a reliable method of determining left ventricular systolic function.111,177–179 Furthermore, several studies have demonstrated that emergency physicians can use visual estimation to accurately assess left ventricular ejection fraction.44,52,73,90,101,180–182

The key to achieving a good outcome includes rapid diagnosis and prompt initiation of therapy to maintain blood pressure and cardiac output. Inotropes are used initially, followed by emergency cardiac catheterization and an intra-aortic balloon pump.316,318 It is important to realize that left ventricular systolic dysfunction can also result from a variety of other etiologies like sepsis, metabolic disturbances, stress cardiomyopathy, or the endpoint of any shock state.110,319–323 Early recognition and aggressive management of shock caused by left ventricular dysfunction are the key to improving mortality.13,117,130,324 Patients with cardiogenic shock have a good prognosis if abnormalities are rapidly diagnosed and aggressively treated.

Some cardiogenic shock patients have a left ventricular outflow obstruction, which can be seen in hypertrophic cardiomyopathy, stress/takotsubo cardiomyopathy, or apical myocardial infarction with hyperkinesis of the remaining myocardium.317 Acute treatment includes volume resuscitation and an intra-aortic balloon pump as needed. Inotropic agents will exacerbate obstruction and may cause rapid deterioration and death. Pure α–agonists may be used to increase afterload and reduce obstruction.317

Mechanical complications of myocardial infarction cause 12% of cases of cardiogenic shock.317 These complications include rupture of the intraventricular septum, free wall, or papillary muscles. Bedside echocardiography can quickly identify most of these abnormalities.56,325 The diagnosis of acute mitral regurgitation requires the use of color flow Doppler and more advanced skill. Acute mitral regurgitation can be caused by papillary muscle/chordae rupture, which is more common with inferior wall myocardial infarction, or left ventricular dilation with expansion of the mitral apparatus. Patients with suspected papillary/chordae rupture should have an urgent surgical consultation.

Hypovolemia is a common finding in hypotensive patients. Point-of-care ultrasound exam of the left ventricle and the IVC can be used to rapidly diagnose hypovolemia. Acute hemorrhage and sepsis are the most common causes of hypovolemia, and early aggressive fluid therapy is the initial management, regardless of the underlying etiology. While initial fluid resuscitation is ongoing, further ultrasound evaluation can help determine the etiology of hemorrhagic shock (see Chapter 5 “Trauma,” Chapter 9 “Abdominal Aortic Aneurysm,” and Chapter 8 “Critical Care”). In patients with septic shock, ongoing fluid requirements can be determined by serial measurements of fluid responsiveness (also see the section “Volume Status and Fluid Responsiveness”).

Hyperdynamic left ventricular function is often seen in hypotensive patients and is generally considered an indicator of hypovolemia. Bedside cardiac ultrasound with a subjective assessment of hyperdynamic cardiac function and left ventricular systolic collapse has been found to be a better indicator of hypovolemia than CVP or IVC size or collapsibility.76,79 In a study using bedside echocardiography to evaluate left ventricular function of ED patients with atraumatic, unexplained hypotension, it was demonstrated that the presence of a hyperdynamic left ventricle was highly specific for sepsis as the etiology of shock.33

Remember that the cardiac exam is only one part of a more comprehensive approach to using point-of-care ultrasound for shock.1,2,49,53,55–57,61,74 (see Chapter 8, “Critical Care”).

Emergency Cardiac Pacing

Transcutaneous cardiac pacing is a common treatment for hemodynamically unstable bradycardias. Application and use of external pacing devices is straightforward, but assessment of mechanical ventricular capture during pacing can be confusing. If the pacing unit is used for electrocardiographic monitoring, then a pacing filter may allow correct assessment of electrical capture. Even with a filter, pacer spikes can drown out the native QRS complexes and give a false impression that there is electrical capture when there is none. An alternative means of assessing the capture is to feel the patients pulse and confirm that pulses correspond to pacer output. However, this can also be difficult especially if pacing causes significant skeletal muscle contractions.24 The use of bedside echocardiography to assess pacemaker capture is straightforward.4 One study showed that determination of mechanical cardiac capture by physicians at the bedside was both reliable and reproducible.326

Bedside echocardiography can also be used to help guide placement of a temporary transvenous pacing catheter. Emergency physicians have used ultrasound guidance to place pacing catheters into the apex of the right ventricle and confirm ventricular mechanical capture with excellent success.4

Valvular Abnormalities

Only severe valvular abnormalities are of interest during a point-of-care cardiac ultrasound exam. Evaluation of the valves generally requires more advanced skill. This is a conundrum, because valvular abnormalities cannot be overlooked. Significant valvular abnormality may be the primary cause of acute hemodynamic compromise, and the ability to detect these abnormalities in a timely manner may be lifesaving. Fortunately, some valvular abnormalities can be detected with 2D inspection and a rudimentary color flow Doppler examination.

Mitral regurgitation, also known as mitral insufficiency, is a common disorder. Chronic mitral regurgitation can be caused by mitral valve prolapse, rheumatic disease, infective endocarditis, or congenital abnormalities. Acute mitral regurgitation is caused by rupture of chordae tendineae or papillary muscles as the result of a myocardial infarction or infective endocarditis.327 Ischemic rupture is most likely to result from an inferior wall myocardial infarction with involvement of the right coronary artery. Acute mitral valve insufficiency causes dyspnea, pulmonary edema, and cardiogenic shock. Rupture of the entire papillary muscle usually results in acute severe mitral regurgitation and cardiogenic shock.328 This process should be suspected in patients presenting with new onset severe pulmonary edema. Rapid diagnosis and emergency surgery are the key to survival for these patients.

Both leaflets of the mitral valve are usually clearly visualized on parasternal long-axis and apical four-chamber views. Normal valve leaflets should appear thin, produce uniform echoes, and be unrestricted in their motion. Thickened, immobile valve leaflets are often associated with regurgitation. Rupture of one of the mitral valve leaflets will usually result in a clearly visible flail leaflet if the entire papillary muscle is ruptured. Color flow Doppler is the key to detecting regurgitation and the easiest way to determine the severity of regurgitation. Mitral regurgitation is severe if the regurgitant jet area fills >40% of the left atrial area (Figure 6-9).329

Aortic regurgitation is an acute process in about 20% of cases and most commonly caused by infective endocarditis or proximal aortic dissection. In acute aortic valve incompetence, left ventricular failure develops rapidly and mortality from pulmonary edema and cardiac arrest is high, even with intensive medical therapy. The key to survival for these patients is rapid recognition of their condition and emergency surgery. Characteristic physical findings, including a murmur, are unreliable in the most severe cases. Cardiac ultrasound is indispensable in identifying the presence and severity of valvular regurgitation.330 Patients with chronic aortic regurgitation are more likely to have obvious abnormalities, such as thickened and immobile leaflets or left ventricular enlargement. Those with acute regurgitation may have a normal-sized left ventricle and thin valve leaflets on 2D imaging. The aortic valve is usually well visualized on the parasternal long-axis view. Normal valve leaflets should appear thin, produce uniform echoes, and be unrestricted in their motion. During diastole the cusps coapt in the center of the aortic root and during systole they snap open and lie parallel to the aortic wall. Screening for aortic regurgitation requires utilization of color flow Doppler. Subjective visualization of a large regurgitant jet may be enough evidence to prompt further investigation. Measurement of the maximal proximal jet width and its ratio to the LVOT diameter is the best screening test for significant aortic regurgitation. A ratio of ≥65% is diagnostic of severe aortic regurgitation.329

Aortic stenosis can cause angina, syncope, and eventually heart failure. Sudden death from dysrhythmias occurs in 25% of such patients. Patients who present with congestive heart failure should be treated with oxygen and diuretics, but nitrates are not well tolerated in patients with severe aortic stenosis as decreasing preload may result in significant hypotension.331 Aortic stenosis is most commonly caused by calcific changes to a congenital bicuspid valve, calcific stenosis of a trileaflet valve, or rheumatic valve disease. In the United States, roughly 50% of aortic stenosis cases are caused by bicuspid aortic valves and the other 50% by calcific stenosis. Rheumatic aortic stenosis is uncommon in the developed world, but common elsewhere. Rheumatic disease almost always affects the mitral valve first, so patients with rheumatic aortic stenosis will likely also have mitral stenosis.

Evidence of aortic stenosis may be apparent from gross inspection of valvular calcification and movements by 2D imaging. Gross inspection of the aortic valve is best done in the parasternal long- and short-axis views. Normal valve leaflets should appear thin, produce uniform echoes, and be unrestricted in their motion. During diastole the cusps coapt in the center of the aortic root and during systole they snap open and lie parallel to the aortic wall. Most patients with aortic stenosis have significant calcifications and thickening of the aortic valve leaflets, restricted mobility, and reduced leaflet separation, which may be easy to identify with 2D imaging. The finding of thickened leaflets alone is not diagnostic of aortic stenosis because 25% of adults over 65 years of age have aortic sclerosis (irregular valve thickening without left ventricular outflow obstruction). Measuring aortic stenosis severity requires continuous wave (CW) Doppler measurements. The simplest measurement of aortic stenosis severity is maximum jet velocity. Maximum jet velocity increases as stenosis severity increases; a velocity of >4 m/s is diagnostic of severe aortic stenosis.332 Other measurements, such as mean transaortic gradient and calculation of valve area using the continuity equation, can also be employed. In addition, severe aortic stenosis usually causes concentric LVH and diffuse left ventricular wall thickening without chamber enlargement.

Significant mitral stenosis is nearly always caused by rheumatic disease.333 This is uncommon in the United States, but developing countries have a high prevalence of rheumatic heart disease. Since the mitral valve is straightforward to visualize in the parasternal and apical views, significant mitral stenosis is usually obvious. Gross inspection of mitral valve opening can usually be seen best in the parasternal long-axis view. The valve opens widely with passive left ventricular filling and again with atrial contraction during diastole. This may be difficult to appreciate when the heart rate is very high, so it is important to slow or freeze images. The mitral valve may not open widely when the left ventricular function is extremely compromised. This is due to poor flow rather than stenosis. The severity of mitral stenosis can be determined by measuring the mitral valve area (MVA) by direct planimetry in the parasternal short-axis view. Normal MVA is 4–6 cm2 and significant or symptomatic mitral stenosis occurs when MVA is <1.5 cm2.332

Right-sided valvular abnormalities are less likely to cause acute decompensation and are less likely to be isolated problems. Most adults have some mild tricuspid regurgitation, which allows measurement of pressure gradients and estimation of right ventricle pressure during routine echocardiographic exams. Significant tricuspid regurgitation is usually due to right ventricular and tricuspid annular dilation due to pulmonary hypertension or right ventricular dysfunction. It may also be caused by endocarditis, carcinoid heart disease, rheumatic disease, or Ebstein's anomaly.329 Tricuspid stenosis is uncommon and often associated with mitral stenosis when caused by rheumatic disease. It may also be caused by carcinoid syndrome (accompanied by significant tricuspid regurgitation), endocarditis, pacemaker-induced adhesions, or lupus. Tricuspid stenosis can be diagnosed by looking for valve thickening, restricted mobility with diastolic doming, reduced leaflet separation, and right atrial enlargement.332

The pulmonary valve is the most difficult to visualize by ultrasound, so it is more practical to look for accompanying abnormalities such as right ventricular enlargement and hypertrophy. Pulmonary stenosis is almost always congenital, so it is unlikely to be a new or isolated problem. Pulmonary regurgitation is most often seen in patients with pulmonary hypertension, which is often associated with dilation of the pulmonary artery, right ventricle, right atrium, and hepatic veins.329

Aortic Dissection

Aortic dissection occurs when the intima is violated, allowing blood to enter the media and dissect between the intimal and adventitial layers. Common sites for tear include the ascending aorta and the region of the ligamentum arteriosum. The Stanford classification categorizes aortic dissection as type A, which involves the ascending aorta, and type B, which involves only the descending aorta.

Aortic dissection and intramural hematoma may be detected by transthoracic echocardiography on parasternal long-axis and suprasternal views. A linear echogenic flap, indicative of aortic dissection, may be seen across the aortic lumen anywhere along its length. In the parasternal long-axis view, the aortic root (proximal ascending aorta) is usually well visualized, but only a small section of the descending aorta is visualized (in cross section) posterior to the heart. The aortic arch can be visualized using the suprasternal view in most patients, but image quality depends on body habitus and operator experience.334–337 A dissection that extends below the diaphragm may be detected with abdominal sonography. Transthoracic ultrasound is very useful if an abnormality is seen, but not sensitive for detecting thoracic aortic dissection, so it should not be used to rule out this diagnosis.

TEE provides much better resolution and visualization of aortic dissection than transthoracic echocardiography and can be used to rule out this diagnosis. Spiral CT, TEE, and magnetic resonance imaging (MRI) have been demonstrated to have comparable sensitivity, and specificity, with accuracy rates approaching 100%.334–337 One study found that all three modalities approach 100% sensitivity; the specificities for spiral CT, TEE, and MRI were 100%, 94%, and 94%, respectively.338

Important issues to address with aortic dissection include (1) presence of pericardial effusion as a sign of imminent mortality without surgical intervention, (2) presence of ascending aorta involvement without pericardial involvement, (3) evidence of isolated descending aorta involvement, (4) location of the entry site, and (5) evidence of involvement of major branch vessels.334–337

Myocardial Ischemia and Infarction

The diagnosis of acute myocardial ischemia can sometimes be made by echocardiographic findings of wall motion abnormalities. Myocardial function is immediately affected by ischemia and may precede ECG changes. Studies have demonstrated that the recognition of regional wall motion abnormalities by echocardiography in patients with acute chest pain is a sensitive predictor for Q-wave myocardial infarction. In experienced hands, the sensitivity for detecting a regional wall motion abnormality in acute myocardial infarction is high, but it may be hard to differentiate between new and old wall motion abnormalities without reviewing prior echocardiograms.339,340 The myocardium is usually thinner at the site of an old wall motion abnormality, but this finding may be subtle, especially when the endocardium is difficult to visualize. Inability to obtain high-quality images and clearly visualize the endocardial border significantly decreases the accuracy of ultrasound for detecting wall motion abnormalities.

Clinicians using bedside echocardiography to identify wall motion abnormalities should be aware that left bundle branch block and a history of cardiac surgery can result in abnormal septal wall motion.341–343 Patients with a left bundle branch block have a characteristic systolic rotating or twisting appearance in the parasternal short-axis view. In addition, patients with right ventricle cardiac pacing often have chronic regional wall motion changes that may be confused with acute abnormalities.344,345

Resting echocardiography in patients with acute chest pain is not sufficiently sensitive for exclusion of cardiac ischemia.346,347 In the ED, however, the combination of resting echocardiography and cardiac enzyme serum markers may be a promising combination for the stratification of patients at risk of complications within the hospital and on discharge.348 The identification of echocardiographic abnormalities may expedite admission for stable patients who are being evaluated in an ED.

Echocardiography plays an important role in the noninvasive evaluation of patients with known myocardial infarction, including evaluation of its complications such as left ventricular systolic dysfunction, development of ventricular septal defects, left ventricular rupture, and mitral regurgitation.325 One study of ED patients reported six cases of myocardial rupture with hemopericardium from acute myocardial infarction with early ventricular rupture. As four of these patients met the criteria for emergency thrombolytic therapy, the emergency management was significantly changed by these findings on the focused echocardiogram.56 Chronic complications such as pericarditis, pericardial effusion, left ventricular aneurysm, and left ventricular thrombus may also be evaluated by echocardiography.

Heart

The heart is a hollow muscular organ, placed between the lungs, and enclosed within the pericardium. It is divided by a septum into two halves, right and left, each half being further subdivided into two cavities, the atrium and the ventricle. Blood flows from the right atrium into the right ventricle through the tricuspid valve. From the right ventricle, unoxygenated blood is carried to the lungs through the pulmonary artery. Blood flows from the left atrium into the left ventricle through the mitral valve. From the left ventricle, oxygenated blood is distributed to the body through the aorta. The outflow tract through the aortic valve into the proximal aorta starts anteriorly and curves posteriorly into the posterior mediastinum next to the esophagus. The aorta is divided into the ascending aorta, the aortic arch, and the descending aorta. The ascending aorta is approximately 5 cm in length; the only branches of the ascending aorta are the coronary arteries. The aortic arch has three branches: the innominate artery, the left common carotid artery, and the left subclavian artery.

The pericardium is composed of the parietal and visceral layers, which normally appose each other without any significant fluid accumulation. The pericardium attaches to the superior left atrium and envelops the proximal aspects of the great vessels.

Thoracic Cavity

The thoracic cavity provides both windows and impediments to the accurate sonographic view of the heart. The heart has very few sonographic windows since ribs, the sternum, and the lungs surround it. Common windows include the parasternal, apical, subcostal, and suprasternal views. The left parasternal interspace allows for small sonographic windows into the mediastinum. The superior aspect of the abdomen also allows for soft-tissue windows via the left lobe of the liver. The heart can shift closer to the chest wall in the left decubitus position.

Cardiac Axes and Scanning Windows

The transducer position for all standard cardiac images is obtained relative to the long and short axis of the heart itself, not the torso. In general, the long axis of the heart is from the right shoulder to the left hip and the short axis is from the left shoulder to right hip (Figure 6-10), but cardiac axes can vary significantly in relation to the torso, depending on body habitus and age.

To obtain the standard transthoracic cardiac views, it is important to understand the three main cardiac axes (long, short, and four-chamber) and three main cardiac windows (subcostal, parasternal, and apical) (Figures 6-11, 6-12, and 6-13).

Novice operators should understand that they can begin using point-of-care cardiac ultrasound for basic applications (pericardial effusion and gross cardiac function) after undergoing fundamental training. Clinically useful information can be obtained by providers with just a few hours of training concentrated on one or two cardiac ultrasound views (subcostal four-chamber and parasternal long axis). Novice operators should not be overwhelmed by the large amount of detail described in this chapter, which is intended for intermediate and advanced users, and as reference material. It is important to understand that most emergency providers use point-of-care cardiac ultrasound very effectively with 2D imaging, visual estimation, and very few specific measurements. Table 6-5 lists basic goals of point-of-care cardiac ultrasound.

Clinicians learning ultrasound may find transthoracic echocardiography difficult to learn initially because of the complex anatomy of the heart and difficulty obtaining standard images due to the surrounding air-filled lungs. It is important to note that the long axis of the heart lies diagonal to the long axis of the torso (Figure 6-10). The long axis of the heart is more horizontal in short obese patients and more vertical in tall thin patients. Standard images of the heart are usually obtained from three anatomic locations on and below the chest wall: the subcostal window, the parasternal window, and the apical window. The heart lies higher in the chest cavity in younger patients, obese patients and those who are supine. It lies lower in the chest cavity in elderly patients, thin patients and those who are sitting upright. The apex is found more medially in normal young patients and more laterally in patients with heart disease. Parasternal and apical images may be very difficult to obtain in patients with hyperexpanded lungs.

While most echocardiographers prefer to scan from the patient's left side, many clinicians scan from the patient's right. Cardiac presets should be selected if available on the machine. Patient positioning and ability to cooperate with inspiratory and expiratory maneuvers are critical to obtaining good images. The subcostal views are best obtained in the supine position, the parasternal views may be acquired in the supine or left lateral decubitus positions, and the apical views are usually best obtained in the left lateral decubitus position. Windows through intercostal spaces can be improved by positioning the patient's left hand behind their head, which may slightly widen the window. Nearly any change in patient position may improve cardiac windows and the ability to obtain good images. Subcostal cardiac images are often better when the patient takes a deep breath, and parasternal and apical views are often better when the patient exhales.

Having proper equipment and equipment settings is critical to obtaining good images. Using a phased array cardiac transducer is better than a curvilinear transducer for echocardiography. The phased array transducer allows imaging between the ribs and is especially important for the parasternal short-axis and all apical views. For transthoracic echocardiographic studies, a transducer with a median frequency of about 3.5 MHz (2.5–5.0 MHz) should be used. Most modern ultrasound machines allow operators to use presets for each particular type of examination. Using cardiac presets will produce the best results. Also, modern machines give the operator the ability to change the frequency range of the ultrasound transducer and activate tissue harmonics with the touch of a button. Testing different frequency ranges and activating tissue harmonics during each examination allows the operator to optimize images.

Overall gain and time-gain compensation are also simple to adjust and can be used to optimize each image. Ideal equipment settings produce images in which the edges of anatomic structures are sharply demarcated and the lumen of the cardiac chambers appear black, not grey.

There are several potential windows and views for echocardiography that will be described in detail below. From a practical standpoint, for clinical decision making in emergency and critical care medicine, often a single window and one or two views will provide the information needed for patient management. It is important, however, for clinicians to learn how to obtain images from all three standard anatomic locations (not just the subcostal window) because in any given patient one window may produce excellent images while the others are less optimal. Every patient has unique anatomy and no one anatomic location allows adequate imaging in all patients.

For cardiac ultrasound the orientation marker (right/left indicator) on the monitor is usually oriented to the right side of the image, which is the opposite of the orientation for abdominal and pelvic imaging. This can be set-up automatically with a cardiac preset or changed manually. Table 6-6 provides a comparison of imaging techniques when using a cardiac preset versus an abdominal/pelvic preset. Regardless of the orientation of the indicator on the monitor, the key is to orient the transducer so as to produce the standard images pictured in this chapter. This facilitates recognition of normal cardiac anatomy and function as well as pathologic findings for the clinician and for any others who may review the images.

Transthoracic Cardiac Views

Subcostal Four-Chamber View

The subcostal views are often the most useful views for point-of-care cardiac ultrasound (Video 6-1 Cardiac Subcostal). Scanning from the subcostal window does not interfere in resuscitative measures such as thoracostomy, CPR, subclavian line insertion, or endotracheal intubation. It is easily learned, repeated, and performed as part of both the cardiac and trauma ultrasound evaluations.

Perform the subcostal views at the subxiphoid position of the abdomen (Figure 6-14A). Hold the transducer at a 15° angle to the chest wall and aim the transducer marker toward the patient's left flank (using a cardiac preset). Angle the transducer up or down depending on the depth of the chest cavity to obtain images of the beating heart. Adjust the depth to visualize the atria at the bottom of the monitor screen. Initial poor-quality images may be improved upon by using an appropriate amount of ultrasound gel, using a shallow angle to the chest wall, moving the transducer to the right to use the left lobe of the liver as a window, and moving off the xiphoid and over to the lower intercostal spaces to image the barrel-chested patient with a larger anterior–posterior diameter.

The subcostal four-chamber view should be seen primarily as a diagonal view of the ventricles, atria, pericardium, and the left lobe of the liver (Figures 6-14B,C). If the transducer is angled less acutely and into the upper abdomen from the subxiphoid position, the left lobe of the liver, IVC, and the hepatic veins will be visualized.

Subcostal Short-Axis View

The subcostal short axis view can be achieved by rotating the ultrasound transducer 90° counterclockwise from the four-chamber view (Figure 6-15). Images will resemble parasternal short axis images and they may provide virtually all of the same information (Figure 6-15). This view is especially useful in patients with COPD because hyperinflation of the lungs moves the heart into the subcostal region and makes parasternal and apical views difficult to obtain.

Subcostal Sagittal View of the IVC

The proximal IVC is found in the subcostal midline sagittal view as it courses posterior to the liver and into the right atrium. It is usually measured about 3–4 cm distal to its junction with the atrium or 2-cm distal to the entry of the hepatic veins (Video 6-2 Cardiac IVC).37,276,349 The anterior–posterior diameter can be measured in the sagittal or transverse plane at any location between the hepatic vein and the left renal vein.37,70,271,350

The transducer is placed over the liver in the midline and aligned with the sagittal plane of the body. Emergency physicians usually align the transducer marker toward the patient's feet (using a cardiac preset) (Figure 6-16A). This will place the atrium/diaphragm on the left side of the screen as is the standard for abdominal longitudinal imaging. Cardiologists orient this image with the transducer marker pointing cephalad and the atrium/diaphragm on the right side of the screen. Either orientation is acceptable and provides identical information. The midline sagittal view provides visualization of the heart, the left lobe of the liver, the IVC, and hepatic veins (Figure 6-16B). This view allows evaluation of the proximal IVC during expiration and inspiration (Figure 6-16C,D). The anterior–posterior diameter of the proximal IVC usually measures about 1.5–2.0 cm during expiration and collapses with inspiration. Collapse of >50% during inspiration is consistent with normal (low) right sided filling pressure.

Although many studies use M-mode to accurately measure IVC size and the magnitude of variations, it should be noted that there is no evidence that it is superior to 2D imaging. Two-dimensional imaging is probably better because it is easier to locate the proper site for measurement in a 2D longitudinal view. In addition, transverse imaging of the IVC is also acceptable, but again it is more difficult to locate the best site for measurement in the transverse plane.

Parasternal Long-Axis View

The parasternal long-axis view is obtained by aligning the ultrasound plane with the long axis of the left ventricle (Figure 6-10 (Video 6-3 Cardiac Parasternal Long Axis). Place the transducer perpendicular to the chest wall at the 3rd or 4th intercostal space immediately to the left of the sternum with the transducer indicator directed toward the right shoulder (using a cardiac preset) (Figure 6-17A). The following structures can be visualized from anterior to posterior on the monitor: right ventricular free wall, right ventricular cavity, intraventricular septum (IVS), left ventricular cavity, and the posterior left ventricular free wall (Figure 6-17B). On the right side of the image the aortic and mitral valves and the proximal aorta and left atrium are usually well visualized. In addition, a transverse view of the descending aorta can usually be seen deep to the left atrium (Figure 6-17C). Rotate the transducer to obtain the best axis to view these structures. Angling and tilting may be needed, but less so than for the short-axis view. Properly adjusting the depth will allow better visualize of pertinent structures. Widening the field of view (sector width) may allow visualization of the left atrium and the entire left ventricle simultaneously.

Parasternal Short-Axis View

The imaging plane for the parasternal short-axis view is oriented from the left shoulder to the right hip (Figure 6-10), and should be obtained in the left 3rd or 4th intercostal space just left of the sternum (Figure 6-18A). If the parasternal long-axis view has already been visualized, obtain the parasternal short-axis views by rotating the transducer marker 90° clockwise toward the left shoulder (using a cardiac preset) (Video 6-4 Cardiac Parasternal Short Axis). With the transducer in this position, several different short-axis views can be obtained by tilting the transducer from the apex to the base (Figure 6-18B). Obtain parasternal short-axis views at the base of the heart, the level of the mitral valve (Figures 6-19A,B), the level of the papillary muscles, and at the apex. The short-axis view at the level of the papillary muscles is an important view because it allows identification of the different walls of the left ventricle (Figures 6-20A,B and 6-78). An ideal short-axis view at the base of the heart (Figures 6-21A,B) visualizes the left atrium, right atrium, tricuspid valve, right ventricle, and pulmonary valve encircling the aortic valve which is seen in cross section in the middle of the image (see the section “Valvular Abnormalities”).

Apical Four-Chamber View

The apical four-chamber view is a coronal view of the heart that visualizes all four chambers in one plane (Video 6-5 Cardiac Apical Four-Chamber). Other apical views include the apical five-chamber view, the apical two-chamber view, and the apical long-axis (three-chamber) view. The apical four-chamber view is the starting point from which all other apical views can be found. Start by placing the transducer at the point of maximal impulse (PMI) on the left lateral chest wall, generally in the 5th intercostal space or lower, and aim the transducer marker toward the left posterior axilla, when using a cardiac preset (Figure 6-22A). Whenever possible, place the patient in the left lateral decubitus position to reduce lung artifact and to bring the heart closer to the chest wall. Some rotation may be needed to allow all four chambers to be visualized. The left ventricle should appear long and bullet shaped in proper apical views. The ventricle may appear short and round (“foreshortened”) with cephalad or medial misplacement of the transducer on the chest wall. On the four-chamber view, the right ventricle with its lateral wall, the IVS (septal wall), the left ventricle with its apex and lateral wall, the two atria, the interatrial septum, and the pulmonary veins will be visualized (Figure 6-22B,C). This view is advantageous for assessing left ventricular function as well as relative chamber sizes.

Doppler studies are often obtained with apical views because blood flow is parallel to the ultrasound beam (moving directly toward or away from the transducer) when the transducer is at the apex. When the image sector is swept anteriorly from the four-chamber view, the left ventricular outflow and aortic valve come into view (five-chamber).

Apical Five-Chamber View

The transducer position and orientation for the apical five-chamber view is nearly identical to the position and orientation for the apical four-chamber view. Beginning from the apical four-chamber view, the transducer is tilted or swept slightly anterior, to allow visualization of the LVOT (proximal aorta and aortic valve), which is the “5th” chamber (Figure 6-23A,B).

This view allows good visualization of the aortic valve and the LVOT in a vertical orientation, which is ideal for measuring blood flow. This is the primary view used for measuring Doppler flow across the LVOT and for calculation of stroke volume and cardiac output. It is also a good view for clinicians who may be confused about right-left orientation when obtaining the apical four-chamber view. When the mitral and aortic valves are both visualized simultaneously, there will be no doubt about which chamber is the left ventricle. Since the aortic valve is anterior to the mitral valve, the difference between the apical four-chamber and apical five-chamber views is just a slight anterior tilting of the transducer. The aortic valve and LVOT will appear in the center of the image between the mitral and tricuspid valves. As noted above, ensure that the transducer is truly at the apex and the left ventricle appears long and bullet-shaped. This will align the LVOT vertically, so that blood flow through the aortic valve is moving directly away from the transducer. This will optimize the accuracy of Doppler flow measurements, which are best when blood flow is directly toward or away from the transducer.

Apical Two-Chamber View

To obtain the apical two-chamber view, first obtain the apical four-chamber view and then rotate the transducer about 60° counterclockwise (Figure 6-24A–C).

This view allows visualization of the anterior and inferior walls of the left ventricle complementing the apical four-chamber view for assessing wall motion and function (Figure 6-24B,C). Further counterclockwise rotation of the transducer from the two-chamber view (additional 30°) will produce the apical long-axis (three-chamber) view.

Apical Long-Axis (Three-Chamber) View

The apical long-axis or three-chamber view is another apical variation that provides essentially the same view as the parasternal long-axis view, but from a different vantage point. First obtain the apical four-chamber view, then rotate counterclockwise beyond the apical two-chamber view until the aortic valve is visualized on the right side of the image (Figures 6-24A and 6-25A–C). Like the apical five-chamber view, this view aligns the mitral valve and LVOT in a vertical orientation. In this position, blood flow in and out of the left ventricle is directly toward and away from the transducer, which is optimal for Doppler flow measurements. The apical long-axis view provides visualization of the same structures as the parasternal long-axis view, including the IVS and posterior wall, with better visualization of the apex.

Suprasternal View

The suprasternal view allows visualization of the aortic arch with its three main branches: the innominate artery, the left carotid artery, and the left subclavian artery. Place the transducer in the sternal notch with the transducer marker pointed toward the patient's left scapula (using a cardiac preset) and the transducer aimed as far anteriorly as possible (Figure 6-26). This view may detect an aortic aneurysm or dissection. The right pulmonary artery, in cross section, can be seen below the aortic arch. If the transducer is rotated 90° to visualize the aortic arch in cross section, the left pulmonary artery may be better visualized. Occasionally, the superior vena cava may be visualized lateral to the ascending aorta.

Most emergency providers use point-of-care cardiac ultrasound effectively without making any specific measurements, using just a visual estimation of cardiac structure and function, and most measurements are not considered part of the basic cardiac ultrasound examination (Table 6-5). Making 2D measurements or using M-mode or Doppler functions may be intimidating for novice operators. Some of the measurement techniques described below are simple to learn and may be used by novices, and some will only be useful for intermediate or advanced providers.

Measurements of Left Ventricular Structure and Function

There are several ways to measure left ventricular structure and function described in the following sections. These include visual estimation of ejection fraction and EPSS, 2D measurements of left ventricle chamber area/volume to calculate ejection fraction, M-mode measurements to calculate ejection fraction and left ventricle mass, and Doppler flow measurements to calculate stroke volume and cardiac output. Most ultrasound machines have software that can calculate these indices with a few simple measurements, but each calculation package is different, so it is important to learn the specifics of your machine's calculation software. Also, while it may be satisfying to calculate a value for ejection fraction, it has been shown that visual estimation of ejection fraction is as good or better than a calculated ejection fraction. Visual estimation is also easier and faster, so it is the most frequent method in clinical use today. Regardless, learning to measure cardiac structure and function is a useful exercise, to improve cardiac ultrasound skills and learn to obtain high-quality standard images. Measurements and visual estimation of ejection fraction will be inaccurate if the cardiac views are oblique, foreshortened, or otherwise of poor quality. Also, regional wall motion abnormalities, tachycardia, and bundle branch blocks can make it difficult to accurately estimate and measure ejection fraction.

Spectral Doppler measurements can be used to calculate stroke volume and cardiac output. It is important to understand that these values provide a different type of information and do not necessarily correlate with ejection fraction. These parameters are rarely measured by emergency physicians, because a single measurement of stroke volume or cardiac output is rarely useful. Only serial or repeat measurements of these parameters, before and after a given treatment, are clinically useful. For example, measuring stroke volume before and after a fluid challenge, or with passive leg raising, can determine whether a patient has a positive hemodynamic effect with fluid resuscitation.

Two-Dimensional Measurements

Measure chamber dimensions and sizes at right angles to the long axis of the respective chamber. Measurement of chamber size, wall thickness, and the left ventricular function may be helpful. By measuring the left ventricular dimensions in systole and diastole, one can calculate the ejection fraction manually or by using the ultrasound machine calculation package. Critical to the 2D measurement is the ability to visualize the endocardium and a cine memory in order to scroll to the correct point in the cardiac cycle for measurement. Table 6-7 lists abnormal cutoff values of common cardiac measurements.

Left Ventricular Diameter and Wall Thickness

Simple linear measurements of the left ventricle can be used to calculate left ventricular mass and ejection fraction (fractional shortening). These measurements are made in the mid-papillary region of the left ventricle, just beyond the tips of the mitral valve leaflets. Simply measuring the IVS, left ventricular internal diameter (LVID), and left ventricular posterior wall (LVPW) in diastole allows calculation of left ventricular mass and diagnosis of concentric or eccentric LVH (Figure 6-27, Table 6-8). Rapid measurements of chamber sizes can be made using 2D images. Simply freeze the 2D image, scroll back through the cine loop to end diastole, and make the appropriate measurements. A visual estimate comparing the chamber or wall to the image scale is often adequate, but calipers can also be used if visual estimation not adequate. The most accurate measurements are often made using M-mode images (see M-mode measurements in following section). If these measurements are made during both diastole and systole, the left ventricular ejection fraction (fractional shortening) can be calculated (see the section “M-Mode” for more details).

Left Ventricular Volumes and Ejection Fraction

Visual estimation is the most efficient method for estimating left ventricular ejection fraction. Simply obtain an apical four-chamber view (or any view for gross estimation) and answer the following question. Does the volume of blood ejected from the left ventricle appear to be >50–55% (normal), 30–50% (mild-to-moderate reduction in ejection fraction), or <25% (severely reduced ejection fraction)? A rough estimate of the patient's left ventricular function can often guide the clinician to appropriate initial treatment, a precise number is not essential. Most quantitative measurements of left ventricular function are considered to be more advanced techniques and may not be appropriate or necessary for basic point-of-care cardiac ultrasound.

Quantitative measurements may be useful for ongoing treatment of critically ill patients and can be accomplished by measuring left ventricle chamber size by tracing the endocardial border in the apical four-chamber and apical two-chamber views. The left ventricular volumes are then calculated by the computer software, which fills the traced area with a stack of elliptical discs and calculates the volume based on that model (Figure 6-28A,B). Ejection fraction measurements are most accurate if the volumes are measured in both the apical four-chamber and apical two-chamber views, but most machines will display ejection fraction if just one view is obtained. It is important to obtain true apical views, so that the left ventricle is long and bullet shaped, not foreshortened or oblique, and a line drawn through the center of the long-axis of the ventricle intersects the center of the transducer. Utilization of this technique may be limited by time constraints and image quality. Even with good views it is often difficult to visualize the endocardial border, and contrast echocardiography significantly improves the accuracy and reproducibility of measuring left ventricular ejection fraction,190,191 especially in obese patients and those with lung disease.192

Aortic Root and Left Atrial Diameter

Simple linear measurements of the aortic root and left atrial diameter (or dimension) are obtained from a parasternal long-axis view (Figure 6-29). The upper limit of normal of the aortic root is 3.5 cm and the upper limit of normal of the left atrium is 4.0 cm. A dilated aortic root can be associated with aortic aneurysm or dissection, but is usually just an age-related change. LAE can often be appreciated with just this single measurement, but a normal atrial diameter does not rule out LAE because the atrium often distends in other dimensions while the AP diameter remains normal.

Left Atrial Area and Volume

Left atrial size is most accurate if it is measured in both the apical four-chamber and apical two-chamber views. Measuring the left atrial volume is ideal but this may not be possible if it is not part of the ultrasound machines calculation package. An alternative is to simply trace the area of the left atrium (Figure 6-30A). The upper limit of normal for left atrial area is 20 cm2. There are several methods for measuring left atrial volume. The biplane area-length measurement of volume involves tracing the atrial border and measuring the length perpendicular from the center of the mitral annulus to the lower aspect of the atrium (Figure 6-30B).

Right Ventricular Dimensions

Right ventricular enlargement is often obvious and no measurements need to be made. The right ventricle is usually smaller than the left ventricle, so a rapid visual comparison of these two chambers in the apical four-chamber view is helpful. When the right ventricle becomes equal or larger in size than the left ventricle, it is easy to recognize right ventricular enlargement. In more subtle cases, it is useful to perform measurements of the right ventricle. Normal measurement of the mid-right ventricle diameter is <3.5 cm and normal measurement of the basal right ventricle diameter is <4 cm. Measurements significantly larger than normal are associated with cor pulmonale (Figure 6-31). Significantly elevated right-sided pressures often cause bowing of the IVS and significant tricuspid regurgitation, so it is useful to look for those findings if the right ventricle is enlarged.

Left Ventricular Outflow Tract

The LVOT diameter is commonly measured in the parasternal long-axis view at the level of the base of the valve leaflets (Figure 6-32). The computer then calculates the cross-sectional area, and this value is one of the variables in the equation for calculating stroke volume (see the section “Stroke Volume”).

M-Mode

M-mode (motion mode) allows for a 1D tracing of structures over time. M-mode can record subtle changes in motion of structures that typically move faster than human vision can perceive. Measurement of valve diameter, wall motion, wall thickness, and stroke volume is possible. There are several uses of M-mode tracing but the most common in point-of-care ultrasound is the tracing through the left ventricle for measurement of left ventricular size and function and to confirm the presence of a pericardial effusion.

E-Point Septal Separation

An M-mode tracing at the mitral valve level in the parasternal long-axis view allows measurement of the right ventricular free wall, IVS, the mitral valve leaflets, the posterior left ventricular wall, and the pericardium. An M-mode tracing through the anterior leaflet of the mitral valve produces a double peak pattern (Figure 6-33A,B). The first peak is the E-point and is caused by passive filling of the left ventricle in early diastole. The second peak is the A-point and is caused by atrial contraction. This double peak pattern is evidence of sinus rhythm. The distance between the E-point and the IVS is EPSS. A large EPSS (in the absence of mitral stenosis) reflects left ventricular systolic dysfunction, left ventricular dilatation, or aortic regurgitation. Normal EPSS is ≤6 mm.187 EPSS >7 mm indicates a ejection fraction of <50% and EPSS ≥13 mm indicates an ejection fraction of ≤35%.186

M-Mode Measurements of Left Ventricular Mass and Left Ventricular Function

Quantitative measurements of these parameters are generally considered more advanced techniques, and these measurements are not considered part of the basic point-of-care cardiac ultrasound exam (Table 6-5). However, understanding these concepts and how easy it is to make M-mode measurements will improve the providers understanding of how to visually assess 2D images in real time.

These measurements can be made in the parasternal long- or short-axis view (Figures 6-34A–D). The M-mode cursor is directed through the left ventricle at the level of the mid-papillary muscles. The measurements of the IVS, LVID, and LVPW are made using the calculation cursor. These simple measurements allow the calculation of left ventricular mass, diagnosis of concentric or eccentric LVH, and fractional shortening/ejection fraction (Figure 6-27, Tables 6-7 and 6-8). Note that determining left ventricular contractility using these measurements is technically called “fractional shortening,” but most modern ultrasound machines report ejection fraction rather than fractional shortening when these measurements are made, because ejection fraction is a more familiar term and there is a linear correlation between ejection fraction and fractional shortening.

M-Mode Assessment of the IVC

M-mode assessment of the IVC allows for visual estimation and measurement of the diameter throughout the respiratory cycle. CVP can be estimated by measuring the diameter and inspiratory changes of the IVC in nonintubated patients (Table 6-4). If CVP is normal (<10 mm Hg), the IVC will collapse >50% with inspiration (Figure 6-35A,B). If CVP is elevated (>10 mm Hg), the IVC will be large (>2 cm) and will not collapse with inspiration (Figure 6-35C).

Measurements of Volume Status and Fluid Responsiveness

There are several methods for determining volume status and fluid responsiveness described in the following sections. The traditional method is to measure the size and collapsibility of the IVC (Table 6-4); however, estimating fluid needs based on IVC indices alone may be oversimplified and can lead to clinical mistakes. Although IVC measurements cannot accurately measure CVP values, they can be used to effectively estimate whether CVP is very low or very high. For example, when the IVC is small (IVCe <1 cm) and collapses with inspiration, it is a good indication that the patient is volume depleted (also see the section “Volume Depletion and Fluid Responsiveness”).

From a practical standpoint, the initial size and respiratory variation in the IVC are not as helpful (except when at the extremes) as the changes that occur in these parameters in response to a fluid challenge. When a patient presents with undifferentiated hypotension, the initial treatment often involves a fluid challenge. Serial monitoring of the IVC can help the clinician evaluate the effect of this treatment more accurately. In general, if the patient's hemodynamics improve and the IVC changes little on ultrasound, more fluid can be given. When IVC measurements indicate a significant or rapid increase in CVP, it may be best to limit fluid therapy. Changes in IVC caliber should also be correlated with the patient's left ventricular function and capacity to accept a volume challenge.

IVC measurements may be helpful for initial determination of volume status and fluid needs, but they are not very useful after initial resuscitation for the ongoing assessment of fluid requirements. In these patients, there is significant evidence that CVP does not correlate with fluid responsiveness. It should be understood that fluid responsiveness is different from CVP (see the section “Volume Status and Fluid Responsiveness”). It is best to use IVC measurements along with other parameters, like changes in stroke volume, which have been proven to predict fluid responsiveness. The only IVC measurement that has been proven to predict fluid responsiveness is IVC distension with mechanical insufflation in intubated patients. In intubated patients, there is no inspiratory collapse, rather mechanical insufflation has the opposite effect (distension); this may be subtle and distension of the IVC by 18% is highly predictive of fluid responsiveness. Another way to predict fluid responsiveness in intubated patients is to measure the stroke volume (or peak flow velocity or VTI) variation caused by changes in intrathoracic pressure during mechanical ventilation. The best way to predict fluid responsiveness with cardiac ultrasound may be to measure the stroke volume (or peak flow velocity or VTI) before and after passive leg raising, because this technique can be used in both intubated and nonintubated patients. This gives the patient an endogenous fluid challenge by significantly increasing venous return and will increase the stroke volume by >15% in patients who are fluid responsive (Figure 6-7A,B,C). See the following section on spectral Doppler measurement of stroke volume, and the section “Volume Depletion and Fluid Responsiveness” under Common and Emergent Abnormalities.

Doppler Principles and Measurements

Doppler ultrasound imaging requires more advanced skill and is not generally considered part of the basic point-of-care cardiac ultrasound exam (Table 6-5); however, some application of Doppler imaging (like transmitral flow) have been shown to be useful in the hands of emergency care providers. Doppler ultrasound uses the “Doppler effect” to identify or quantitate movement. The Doppler effect (or Doppler shift), named after Austrian physicist Christian Doppler, is the change in frequency as the source of the sound signal moves relative to the receiver. Using this principle, Doppler ultrasound can be used to identify and quantify movement of blood or tissue. Doppler ultrasound is most sensitive and accurate when movement of blood or tissue is directly toward or away from the transducer. The sampling beam must be positioned as close as possible to the direction of flow, since angle-correction is generally not used for cardiac Doppler measurements. Movement of blood or tissue can be displayed using a color display or as a waveform on a spectral display.

Color Doppler

Color Doppler flow imaging is used to visualize blood flow, and blood of different velocities and direction is assigned different colors. By convention, red represents flow toward the transducer and blue represents flow away from the transducer (Figure 6-36). It should be noted that the red and blue colors do not necessarily signify arterial or venous flow or specific vessels. In addition, degrees of velocity are mapped as shades of red and blue. Shades of orange, green, or yellow may represent degrees of velocity, variance, or turbulence. Optimizing the color flow image is accomplished by using the highest possible velocity scale. Decreasing the size of the color box increases pulse repetition frequency and allows more accurate depiction of high-frequency flow without artifacts. Color Doppler is used mostly for determining the presence and severity of valve regurgitation. The length and width of the color jet are factors in determining the severity of valve regurgitation (see the section “Valvular Abnormalities”).

Spectral Doppler

Spectral Doppler is a type of ultrasound image display in which flow velocity and direction are represented on the Y-axis and time is represented on the X-axis. Pulsed wave (PW) Doppler, CW Doppler, and tissue Doppler imaging (TDI) are displayed in this manner. PW Doppler is used to measure flow through the LVOT to calculate the left ventricular stroke volume and to document transmitral flow patterns to evaluate left ventricular diastolic function. CW Doppler is used to measure higher flow rates through stenotic or regurgitant valves, and is commonly used to measure tricuspid regurgitation to estimate right ventricular systolic pressure (RVSP) and to measure flow rates through stenotic lesions for valve area calculations. TDI is used to measure the movement of the mitral annulus during diastole, to assess left ventricular diastolic function.

Stroke Volume

Left ventricular stroke volume is determined by measuring the area of the LVOT and the Doppler flow through the LVOT. The cross-sectional area of the LVOT is calculated from a simple linear measurement (Figure 6-32). Blood flow through the LVOT is measured using pulsed Doppler, using the apical five-chamber or apical long-axis view (Figure 6-37A). The Doppler waveform is traced and the computer calculates the VTI (Figure 6-37B). The product of the VTI and the cross-sectional area of the LVOT is equal to the stroke volume (Table 6-8).

Vpeak (or Vmax) is the peak velocity of the pulsed Doppler blood flow and has a linear correlation with stroke volume. Visual estimation or measurements of changes in Vpeak, after passive leg raising, with respirations or after a fluid challenge, may be helpful in predicting fluid responsiveness.

Transmitral Flow

Transmitral Doppler flow is measured to determine left ventricular diastolic function. Pulsed Doppler is used in the apical four-chamber view, and the measuring gate is placed just inside the left ventricle beyond the tips of the mitral valve leaflets. Two distinct Doppler waveforms are created during diastole, corresponding with passive filling of the left ventricle and the atrial contraction. In a normal healthy heart, the majority of left ventricular filling occurs passively in early diastole (E-wave) and a small amount of filling occurs with atrial contraction (A-wave) (Figure 6-38A). The most important aspects of transmitral flow are the E/A pattern, the E/A ratio, and the measurement of the deceleration time of the E-wave (Figure 6-38B). The E/A ratio is normally 1–2 and the deceleration time is normally 160–240 ms (see the section “Diastolic Dysfunction” for abnormal filling patterns).

Right Ventricular Systolic Pressure

Measurement of the peak velocity of tricuspid regurgitation is used to calculate RVSP. This is usually done using CW Doppler, but pulsed Doppler can also be used. The Doppler measuring gate is placed into the regurgitation jet using 2D and color Doppler flow guidance (Figure 6-39). The maximal velocity of regurgitant flow is measured (Vmax) and used to calculate RVSP from estimation of the right atrial pressure (RAP) (Table 6-8).

Cardiac Arrest

Asystole and true EMD are seen as a lack of myocardial contractions on ultrasound. Pooling of blood may be seen and echogenic clots may be formed under these conditions (Figure 6-40). A subjective assessment of the presence or absence of coordinated myocardial contractions (or kinetic wall motion) and an assessment of left ventricular function often change clinical management and are important prognostic indicators.8,13,130 Movement of the valves can be seen just with positive pressure ventilation and should not be mistaken for spontaneous circulation in the absence of myocardial contractions.

Cardiac Tamponade

Cardiac tamponade is not dependent on the amount of fluid in the pericardial sac but on the rate of fluid accumulation within the pericardial sac (Figure 6-2). Emergent echocardiographic findings of cardiac tamponade include a pericardial effusion, right atrial collapse during ventricular systole, right ventricular diastolic collapse (Figures 6-41 and 6-42), and lack of respiratory variation in the IVC and hepatic veins. Rarely, tamponade may present with isolated left atrial or left ventricular collapse in patients with loculated effusions or severe pulmonary hypertension.

Pericardial Effusion

Pericardial effusion is typically characterized by an anechoic fluid collection between the parietal pericardium and the visceral pericardium (Figures 6-43A,B and 6-44). For all practical purposes, the visceral pericardium is not visualized by transthoracic echocardiography. However, the combined interface of the parietal and visceral pericardium is echogenic.

On transthoracic echocardiography, pericardial effusions may be judged as small or large. Small pericardial effusions are seen as an anechoic space <1 cm thick and are often localized, usually between the posterior pericardium and left ventricular epicardium. Large effusions are seen as an anechoic space >1.5 cm thick, and usually completely surround the heart. In patients with larger effusions, the heart may swing freely within the pericardial sac (Figure 6-45).

Pericardial volumes of up to 50 mL may be normal; however, pathologic fluid collections, if slow in progression, may accumulate hundreds of milliliters. Pericardial fluid is usually anechoic, but exudative effu-sions, such as pus, malignant effusions, and blood mixed with fibrin material, may be echogenic (Figure 6-46).

Massive Pulmonary Embolism

While direct visualization of a thrombus may occasionally be seen in the right heart, most echocardiographically detectable changes are indirect indices of right heart strain caused by pumping against a fixed blood clot in the lung. These changes include right ventricular dilatation, right ventricular hypokinesis, tricuspid regurgitation, and abnormal septal motion. The normal right ventricular end-diastolic diameter measured in the apical four-chamber is ≤3.5 at the mid-right ventricle and ≤4.0 at the base of the ventricle (Figure 6-47). The normal right to left ventricle ratio is not consistently defined, but a ratio of 0.5–1.0 is generally considered normal and a ratio of >1.0 is seen with significant right ventricular enlargement.

With massive PE, the right ventricle will be significantly larger than the left ventricle and may be round in shape (Figures 6-3 and 6-48). McConnell's sign, described as diffuse hypokinesis of the right ventricular free wall with apical sparing, is a very specific but insensitive indicator of PE.351 In addition to right-sided heart strain, a blood clot in the lung may cause decreased venous return to the left heart. This may result in decreased LVEDD as well as “paradoxical septal motion.” The normal IVS relaxes outward (toward the right ventricle) in diastole. With increased right end-diastolic pressures and decreased left-sided pressures, abnormal motion of the septum in diastole may be visualized. While this septal deviation toward the left ventricle (also described as “septal flattening” or “D-sign”) may also be observed in systole, its presence is more pronounced in diastole and is especially prominent in the acute phase of massive PE (Figure 6-49).

Tricuspid regurgitation may occur when pulmonary artery pressures exceed right ventricular end-diastolic (right atrial) pressures. Measurement of tricuspid regurgitation requires spectral Doppler velocity measurement and is usually obtained on the apical four-chamber view. This value is used to calculate the pressure gradient between the right atrium and right ventricle (Table 6-8). While many healthy persons have a trivial degree of tricuspid regurgitation, up to 90% of patients with PE will have measurable tricuspid regurgitation. Normal pulmonary artery systolic pressure is approximately 25 mm Hg in a healthy person, corresponding to a regurgitant jet of <2 m/s. Over 3 m/s would correspond to a pulmonary artery pressure of 46 mm Hg. Studies using cutoff values for diagnosis of PE typically cite velocities over 2.5–2.7 m/s as being elevated (Figure 6-50).

All of the indirect indicators of right-sided heart strain may occur in conditions other than PE. These conditions include right ventricular infarct, emphysema, and primary pulmonary hypertension. It is worthwhile to note that the acutely strained right-sided heart rarely has the muscle mass to elevate pulmonary artery pressure into an extremely high range and values well over 40 mm Hg should suggest a chronic elevation. An increase in muscle mass on measurement of the right ventricular free wall may also indicate a more chronic etiology for right ventricular strain as opposed to a thin, acutely dilated right ventricle. The normal thickness of the right ventricular free wall is 2.4 ± 0.5 mm, and it is generally considered hypertrophied at measurements of 5 mm or greater.

Left Ventricular Systolic Dysfunction

Visual estimation is the best way to determine left ventricular function in the emergent setting. It is best to visualize the left ventricle in multiple views (at least two), so that the function of the entire ventricle can be accurately assessed (Figure 6-51). Also, it is best to use a combination of findings to get the most accurate picture of overall cardiac function, including visual estimation of left ventricular function, EPSS, visual inspection of the valves, IVC size and collapsibility, pulmonary ultrasound findings, and simple measurements of systolic or diastolic function.

EPSS provides an objective measure of left ventricular function and is particularly important for those who are inexperienced with visual estimation of left ventricular function. Abnormally large EPSS is consistent with left ventricular dysfunction and increasing EPSS correlates with worsening dysfunction (Figure 6-52). Normal EPSS is ≤6 mm.187 EPSS >7 mm indicates a ejection fraction of <50% and EPSS ≥13 mm indicates an ejection fraction of ≤35%.186

Left ventricular dysfunction can also be measured and documented by measuring the change in left ventricular volume between diastole and systole (Figure 6-53). Volumes are calculated using the method of discs/modified Simpson's rule after tracing the endocardial border. Calculations are most accurate if measurements are performed in both apical four-chamber and two-chamber views.

Left Ventricular Diastolic Dysfunction

Half of all patients with clinical heart failure have isolated diastolic dysfunction with normal left ventricular systolic function. Older patients with hypertension and LVH tend to have diastolic dysfunction. Also, diastolic dysfunction is the most common cause of LAE. Therefore, looking for LVH and LAE is part of assessing for diastolic dysfunction (see the sections “Left Ventricular Hypertrophy” and “Left Atrial Enlargement” for more details). Doppler imaging of left ventricular filling (referred to as transmitral flow or mitral inflow) and TDI of the mitral annulus are widely used to identify and determine the severity of diastolic dysfunction, and both techniques can be used by emergency physicians (Figure 6-54).45,48

Transmitral flow is measured by pulsed Doppler in the apical four-chamber or apical two-chamber view. The measuring gate is placed just inside the left ventricle at the tips of the mitral valve leaflets. There are two components to ventricular filling during diastole; early passive diastolic filling (E-wave) and late diastolic filling caused by the atrial contraction (A-wave). In a normal heart, without diastolic dysfunction, most of the ventricular filling occurs during early diastole, so E is larger than A, with an E/A ratio of 1–2 (Figure 6-38A). With early diastolic dysfunction (impaired relaxation), there is a reversal of the characteristic E/A pattern and E is smaller than A (Figure 6-55A). Also, impaired relaxation may cause prolongation (>240 ms) of the deceleration time of the E-wave (Figure 6-54). With worsening diastolic dysfunction, the E/A ratio reverses again, with E larger than A, which is referred to as “pseudonormalization” (Figure 6-55B). A pseudonormal E/A pattern may be differentiated from a normal E/A pattern by measurement of an abnormally short deceleration time (<160 ms) or by measurement of decreased movement of the mitral annulus (using TDI) during early diastole (see below). Severe diastolic dysfunction is characterized by a restrictive filling pattern, with an E-wave much taller than the A-wave (E/A ratio >2) and a very short deceleration time (Figure 6-55C).

Movement of the mitral annulus is measured by obtaining an apical four-chamber view and placing the TDI gate over the septal portion of the mitral annulus. With normal left ventricular filling, the mitral annulus moves rapidly downward at a velocity of >8 cm/s and this movement is easily measured by TDI and referred to as e' (Figure 6-54). An e' of < 8 cm/s is diagnostic of diastolic dysfunction (Figure 6-56).

Left Ventricular Hypertrophy

LVH may be concentric or eccentric. Patients with concentric hypertrophy have thick left ventricular walls and patients with eccentric hypertrophy have a large LVID. In patients with very thick left ventricle walls (Figure 6-57A), or a very large LVID, the diagnosis may be obvious without measurements. Measurements of left ventricular wall thickness >12 mm or LVID >5.3 cm in females or >5.9 cm in males (in diastole) are findings consistent with LVH (Figure 6-57B and Table 6-7). The most common way to make the diagnosis of LVH is to measure the left ventricular mass (using the area-length or the truncated-ellipse method) and divide it by the body mass index; however, this is somewhat cumbersome and requires the proper calculation software. A simpler way of identifying and classifying LVH is to use a nomogram (Figure 6-58). Measurements of the IVS, LVID, and LVPW are made during diastole using M-mode (Figure 6-57C) and applied to the nomogram (Figure 6-58).

Hypertrophic cardiomyopathy is the leading cause of sudden cardiac death in preadolescent and adolescent children. This entity can be separated into obstructive and nonobstructive types (Figures 6-59 and 6-60). Patients with asymmetric septal hypertrophy (obstructive type) are at risk of dynamic obstruction of the LVOT. However, patients with or without asymmetric septal hypertrophy are at high risk of arrhythmogenic sudden death.

Left Atrial Enlargement

LAE is a significant abnormality that is associated with high left ventricular filling pressure and often caused by diastolic dysfunction or mitral regurgitation. The easiest way to document LAE is to measure the left atrial diameter (dimension) in the parasternal long-axis view during systole (when it is largest). Left atrial diameter >4.0 cm is consistent with LAE (Figure 6-61). The most accurate way to diagnose LAE is to measure the volume using both apical four-chamber and apical two-chamber views (Figure 6-30), but severe LAE may be obvious (Figure 6-62).

Volume Depletion and Fluid Responsiveness

Signs of significant volume depletion on cardiac ultrasound are a hyperdynamic left ventricle with a small left ventricular end-diastolic area (<10 cm2) and/or complete obliteration of the left ventricle during systole (Figure 6-63). A small IVC that measures <10 mm in diameter at its largest during the respiratory cycle (during expiration in spontaneously breathing patients and during insufflation in ventilated patients) is also consistent with significant volume depletion (Figure 6-64).

It is important to understand the concept of fluid responsiveness and why predicting fluid responsiveness is different from estimating CVP. The definition of fluid responsiveness is a positive hemodynamic response (increase in stroke volume of ≥15%) with a fluid bolus of 500 mL of crystalloid. The importance of differentiating between fluid responsiveness and CVP is based on the recognition that excess fluid can be harmful and that only about half of patients with septic shock have a positive hemodynamic response to a fluid bolus. In addition, CVP has been proven to be a poor predictor of fluid responsiveness. Parameters that have been shown to be good predictors of fluid responsiveness are an increase in the diameter (distensibility) of the IVC of >18% with insufflation in mechanically ventilated patients, stroke volume variation of >12% with the respiratory cycle in mechanically ventilated patients, and an increase in stroke volume of >15% with passive leg raising in both ventilated and spontaneously breathing patients (Figures 6-65, 6-66 and 6-7).

Valvular Abnormalities

Patients with valvular abnormalities may be asymptomatic with incidental abnormal findings, symptomatic from acute decompensation from a chronic valve abnormality, or hemodynamically unstable from an acute severe valvular abnormality (usually acute regurgitation). A severe acute valve abnormality may be difficult to recognize because the heart may look grossly normal or just hyperdynamic. Acute mitral regurgitation may result from rupture of a chorda tendinea or papillary muscle and acute aortic regurgitation may be associated with proximal aortic dissection. Chronic severe valvular abnormalities are often associated with significant cardiac dysfunction and chamber enlargement, so it is prudent to consider assessing valvular function in patients with these findings.

Valvular Stenosis

The initial evaluation for valvular stenosis can be accomplished using visual estimation. If good-quality images are obtained, valve opening can be well visualized and significant mitral and aortic stenosis can be ruled out very quickly.

Ruling out aortic stenosis may be straightforward if good 2D images of the aortic valve are obtained. Two cusps of the aortic valve (right coronary cusp and noncoronary cusp) are usually well visualized on the parasternal long-axis view, and a widely opened valve is easy to recognize (Figure 6-32). In the parasternal short-axis view, all three cusps of the aortic valve may be visualized in both the opened and closed position (Figure 6-67). It is important to visualize the valve in the opened position when trying to rule out a bicuspid valve because bicuspid aortic valves often have fusion of the right and left coronary cusps with a raphe replacing the inferior commissure, so the valve may look normal in the closed position (Figure 6-67A). Stenotic valves usually have significant thickening and calcification, so a grossly abnormal valve should increase suspicion for stenosis. However, significant aortic thickening and calcific changes are present in about 25% of elderly patients, and the incidence of aortic stenosis is only a few percent, so most patients with these findings do not have aortic stenosis.

Calculation of the aortic valve area is usually accomplished with CW Doppler measurements at the level of the valve orifice and at the level of the LVOT. These measurements are placed into the continuity equation and the valve area is calculated (Table 6-8). An aortic valve area of 1.0–1.5 cm2 is consistent with mild aortic stenosis, an area of 0.75–1.0 cm2 is consistent with moderate stenosis, and an area <0.75 cm2 is consistent with severe stenosis.

Potentially easier methods for determining significant aortic stenosis are to measure the maximal aortic jet velocity with CW Doppler or the maximal aortic cusp separation using M-mode imaging. Maximal jet velocity is the single highest velocity jet of flow that can be measured in the aortic valve region from any window using CW Doppler. A maximum jet velocity of 3–4 m/s is consistent with mild aortic stenosis and a maximal jet velocity >4 m/s is diagnostic of severe aortic stenosis.332 Assessment of the aortic valve area by measurement of the maximal aortic cusp separation requires a good-quality parasternal long-axis view with the open valve cusps and proximal aorta aligned horizontally on the ultrasound image. Place the M-mode cursor through the aortic valve cusps. Normal aortic valve cusps are in close proximity to the walls of the proximal aorta when the valve is open and meet in the middle of the aorta when the valve is closed, giving a distinct M-mode pattern (Figure 6-68). Maximal aortic cusp separation >15 mm is normal, 12–15 mm is consistent with mild aortic stenosis, and <8 is consistent with severe aortic stenosis.352

Visual estimation to assess for mitral stenosis is usually straightforward. The mitral valve is often best visualized in the parasternal long-axis view and a widely opened valve is easy to recognize (Figure 6-69A). In addition, the area of the mitral valve orifice can easily be measured by 2D planimetry. To measure the valve with planimetry, a parasternal short-axis view is obtained and the mitral valve is traced at the point of maximal opening, at the level of the tips of the mitral valve (Figure 6-69B). Normal MVA is 4–6 cm2, a valve area 1.0–1.5 cm2 is consistent with moderate stenosis, and an area <1.0 cm2 is considered severe stenosis. It is important to realize that decreased left ventricular function causes decreased mitral valve opening, which is why EPSS is useful (Figure 6-52A). Therefore, providers must differentiate mitral stenosis from severe left ventricular dysfunction by assessing the ventricle and the appearance of the valve during diastole. A stenotic mitral valve has a distinctive appearance with ballooning and a “hockey stick” shaped anterior leaflet during diastole (see Figure 6-90B).

Several genetic valvular anomalies may be easy to recognize with visual inspection of valve location and movement, and by recognition of abnormal chamber sizes (Figure 6-70).

Valvular Regurgitation

Color Doppler is the primary initial ultrasound test for valvular regurgitation. The angle of interrogation and the scale are the two most important factors when screening for regurgitant flow with color Doppler imaging. The color scale is optimal when it is adjusted to the highest possible velocity that still allows visualization of the regurgitation jet. Decreasing the size of the sampling box will allow the scale to be increased. The mitral valve is best evaluated in the apical four-chamber view or the parasternal long-axis view, the aortic valve is best evaluated in the parasternal long-axis view, the tricuspid valve can be evaluated in the apical four-chamber view or the parasternal short-axis view, and the pulmonary valve can be evaluated in the parasternal short-axis view.

Color Doppler can also be used to judge the severity of valve regurgitation. Normal so-called “physiologic” regurgitation (with a short thin regurgitant jet) is commonly seen in the mitral and tricuspid valves in normal healthy individuals, and is clinically insignificant. Moderate or severe mitral and tricuspid regurgitation is consistent with a large regurgitant jet area (a long, wide jet). Regurgitant jets that occupy >40% of the atrial area and/or extend to the opposite wall of the atria are considered severe (Figures 6-71 and 6-72). Aortic regurgitation is rare in normal healthy individuals. Aortic regurgitation is best seen in the parasternal long-axis view. The severity of aortic regurgitation is based on the regurgitant jet height (width) and the ratio of the jet height to the height (width) of the LVOT. Regurgitant jets that occupy >65% of the height of the LVOT are considered severe (Figure 6-73).

Placement of Emergency Cardiac Pacemaker

Please see Chapter 8 “Critical Care” for discussion.

Myocardial Ischemia

Abnormal wall motion and abnormal ventricular emptying or relaxation characterizes left ventricular dysfunction. Ultrasound findings of acute left ventricular ischemia or infarction typically include wall motion abnormalities, usually regional in the distribution of a coronary artery or its branch, but without evidence of chronic thinning or scarring of the wall (Figure 6-74). Wall motion is graded as hypokinesis (reduced ventricular wall thickening and motion), akinesis (absent wall thickening and motion), and dyskinesia (paradoxical motion of the wall—outward movement of the wall during systole). 92,102 Ultrasound findings of chronic left ventricular infarction include a dilated left ventricle, global wall motion abnormalities with thinning of the ventricular wall (<7 mm or 30% less than the adjacent normal wall), and increased echogenicity of the segment due to fibrotic changes (Figure 6-75A,B).

Assessment of wall thickening requires ultrasound visualization of the myocardium and endocardium, which can be significantly limited for the typical emergency or critically ill patient. Contrast echocardiography provides a much better assessment of global and regional wall motion and has been proven to be very useful for assessing regional wall motion in ED patients with chest pain and potential acute coronary syndrome.353–355 Wall motion may be characterized by gross ventricular wall dysfunction or segmental wall motion defects that usually follow the distribution of coronary vasculature (Figures 6-76 and 6-77). Multiple views of the left ventricle and a knowledge of the coronary vascular anatomy are required if the goal is to determine the region affected and correlate findings with the ECG (Figure 6-78A–D). In addition to improving visualization of the endocardial border and the myocardium, infusion of IV contrast also allows for assessment of regional myocardial perfusion, which provides significant additional information and value in the evaluation of patients presenting to the ED with chest pain.354

Proximal Aortic Dissection

Patients with a proximal thoracic aortic dissection often have a dilated aortic root (>3.5 cm), which is easily visualized on the parasternal long-axis view. An intimal flap can sometimes be seen within the dilated aortic root (Figure 6-79). The descending aorta may also be seen on the parasternal long-axis view in cross section posterior to the mitral valve. The arch of the aorta may be seen with transthoracic echocardiography using a suprasternal window. A dissection within the aortic arch or descending thoracic aorta may be seen in this view (Figure 6-80). In addition to the linear flap, aortic dissection is characterized on echocardiography as having two lumens, true and false, with different flow patterns. This may be best demonstrated using transesophageal views.

Ascending Aortic Aneurysm

Dilation of the ascending aorta over 1.5 times the normal segment may reflect an aneurysmal change (Figure 6-81). A true aneurysm of the ascending aorta involves all layers of the vessel wall. A false aneurysm, or pseudoaneurysm, involves a penetration of the intima and media layers only. Most thoracic aneurysms are fusiform but may be saccular. Concomitant aortic dissection may occur as well.

On echocardiography, the aorta is usually measured at several locations: aortic annulus, aortic leaflet tips, ascending aorta, aortic arch, and descending aorta. Note the length and levels of dilatation. As with the abdominal aorta, if the thoracic aorta diameter is measured at 5–6 cm, then obtain cardiothoracic surgery consultation.

The role of transthoracic echocardiography is limited as the aortic arch and descending aorta cannot be fully visualized because of the depth of the aorta in many views. There is also difficulty in viewing the endothelium and poor windows due to intervening bone and air. TEE, CT, and MRI are similar in accuracy for the detection and evaluation of aortic aneurysm and should be ordered if further evaluation is needed beyond transthoracic echocardiography.

Thrombus

While a thrombus may develop in any cardiac chamber, those with low pressure and low flow are at greater risk of developing a thrombus. A thrombus may be hyperechoic, isoechoic, and even hypoechoic in appearance (Figure 6-82). It is usually laminated with the layers paralleling the chamber wall. A thrombus is typically homogeneous with irregular borders, and may fill in the apex of a ventricle or attach itself to a chamber wall or valves of the atria. Near-field or time-gain compensation may have to be adjusted to visualize suspected areas.

Higher-frequency transducers that utilize cardiac scanning windows close to the cardiac chamber in question provide the best imaging. While transesophageal transducers are required for thrombus detection in atria, transthoracic scanning is adequate for thrombus detection within the ventricles in many cases. If color Doppler is available, the swirling vortices of flow may indicate the presence of a thrombus. Normal structures, such as the left atrial appendages, right atrial Chiari network, and right ventricular moderator bands must be distinguished from thrombus.

Vegetations

Findings of irregularities on valvular surfaces should prompt further investigation and consultation for more definitive diagnosis (Figures 6-83 and 6-84). Vegetations may be echogenic or isoechoic and have an irregular appearance. Vegetations may be seen on any valve leaflet or part of the apparatus. Laminated or pedunculated attachments to the leaflet of the valve should prompt suspicion. In general, vegetations do not restrict valvular motion but some valve leaflets may not coapt together correctly. Typical appearance of normal valves includes smooth echogenic leaflets. Refer all suspected cases for TEE and cardiology consultation.

Myxoma

Myxomas, which are uncommon benign fibrous tumors, are usually attached to a septal wall. Myxomas are usually echogenic, globular, and smooth. They are pedunculated with a stalk on one wall that may or may not be visualized. They are usually attached to an atrial wall, most often the left atrium (Figure 6-85A,B).

1. Contraindications. No contraindications exist to transthoracic echocardiography unless its use is interfering with lifesaving procedures and treatments.

2. Inability to obtain adequate views. Some patients cannot be imaged well by transthoracic echocardiography. These include patients with subcutaneous emphysema, pneumopericardium, large anterior–posterior girth, and chest wall deformities. Suggestions for improving image acquisition include maintaining transducer contact with the chest wall; use of an adequate amount of conduction gel; use of adjacent cardiac windows; and angling, rotating, and tilting the transducer, as necessary. The patient may be turned in the left lateral decubitus position to bring the heart closer to the anterior chest wall.

   • a. The subcostal window is a mainstay of the emergency cardiac ultrasound examination during resuscitation of a critically ill patient. Suggestions for improving image acquisition for this view include ensuring the transducer is at a shallow angle to the plane of the body (15° in general) and moving the transducer to the patient's right in the subcostal space instead of the more intuitive left side. This helps to avoid the air-filled stomach and uses the left lobe of the liver as a soft-tissue window. Also, asking the patient to take a deep inspiration or, if the patient is intubated, providing a large tidal volume will help push the heart toward the subcostal space.
   • b. The parasternal view is often limited by retrosternal air or altered anatomy. Moving the transducer to the left, and then up and down along the anterior–posterior axis may help with obtaining an improved view.
   • c. The apical view may be improved by changing the angle and aiming the transducer toward the head or right elbow instead of the right shoulder.

3. Reversed orientation. Proper imaging requires knowledge of the orientation of the transducer. Reversed orientation may lead the clinician to mistake ventricular enlargement for normal and vice versa. For example, a dilated right ventricle is an important clue for massive PE, but may be falsely identified as normal if a normal left ventricle is viewed on the reversed side of the monitor screen. When ventricle sizes are similar, the right ventricle can be identified on apical four-chamber view by recognizing that the tricuspid valve is positioned closer to the apex than the mitral valve. Another simple technique for confirming proper orientation with the apical four-chamber view is to tilt the transducer anteriorly to visualize the aortic outflow tract, thus obtaining the apical five-chamber view (Figure 6-86).

4. Fluid versus blood clot or fat. Fluid (serous pericardial fluid, or defibrinated blood) will appear anechoic. However, a blood clot may be echogenic initially (Figure 6-87). The borders of clot usually have a thin anechoic stripe. Viewing other windows may assist with identifying free fluid in other aspects of the pericardium. Fat is commonly located in the anterior precordial space. In some patients, this appears hypoechoic and can be mistaken for fluid or hematoma. Clues to identification are mildly echogenic septations characteristic of fat and the lack of any dependent pooling of fluid within the posterior pericardial space.

5. Gain issues. Gain should be adjusted to allow the posterior aspect of the heart to have the highest time-gain compensation. Cardiac chambers should be anechoic and cardiac structures should be echogenic.

6. Depth. Adjust depth to visualize posterior to the cardiac structure in question. Place the focus, if adjustable, at the structure of interest. Too much magnification can alter proper interpretation and too shallow depth can minimize pathologic findings. The clinician might miss a large pericardial effusion if the depth is not adequate to capture the entire heart and the large fluid stripe between the right ventricular wall and diaphragm in the subcostal view is mistaken for the right ventricle.

7. Dynamic range. Many machines used for point-of-care ultrasound are preset for abdominal applications; this includes the dynamic range setting. In cardiac ultrasound, the image is more black and white. The dynamic range should be lower than the settings used in abdominal or pelvic imaging.

Case 1

Patient Presentation

A 64-year-old woman presented to the ED by ambulance in severe respiratory distress. A nebulized albuterol treatment was in progress. She told paramedics that her shortness of breath had become progressively worse over the last several hours. She denied chest pain and any history of cardiac or pulmonary disease. The paramedics communicated that her respiratory distress was worsening.

On physical examination, her respiratory rate was 50–60 breaths per minute and she was using all accessory muscles. She could only speak in two- or three-word sentences due to her dyspnea. Her blood pressure was 161/101 mm Hg, heart rate 136 beats per minute, and oxygen saturation 94% despite receiving 100% supplemental oxygen by nonrebreather mask. Her temperature was normal. Auscultation of her chest revealed diffuse expiratory wheezes, decreased aeration, and a prolonged expiratory phase. There were no crackles appreciated. CV examination revealed tachycardia without murmurs and strong, equal peripheral pulses. Neck examination was without any noticeable jugular venous distention. Lower extremity edema was absent. The remainder of her examination was unremarkable.

Management Course

Two minutes after arrival, a bedside echocardiogram was performed and interpreted by the emergency physician. Notable findings were a dilated left ventricle with obvious severe left ventricular failure and a relatively small right ventricle (Figure 6-88A). The nebulization treatment was stopped and she was given high-flow oxygen and sublingual nitroglycerin. The patient received an IV bolus of furosemide and an IV nitroglycerin infusion was started. By the time her portable chest radiograph was available for viewing (Figure 6-88B) about 15 minutes after arrival, the patient's clinical condition had markedly improved. The chest radiograph confirmed the diagnosis of acute pulmonary edema. An ECG showed sinus tachycardia with nonspecific changes. She was admitted to the cardiac ICU and eventually diagnosed with severe diffuse ischemic cardiomyopathy.

Commentary

Bedside echocardiography was an important tool in the evaluation of this patient's undifferentiated respiratory distress. The course of treatment delivered to this critically ill patient in the ED was significantly altered by the information provided by bedside echocardiography. Even though the patient could not tolerate lying flat, subcostal transducer positioning provided adequate visualization of her left ventricular dysfunction. This vital piece of information would not have been detectable by any other diagnostic modality within 2 minutes of the patient's arrival.

Case 2

Patient Presentation

A 52-year-old man presented to the ED with vague, nonradiating chest pain over the previous 2–3 hours, gradual in onset over about 30 minutes. The patient had not experienced any significant shortness of breath, nausea, or palpitations. He acknowledged a history of inconsistently controlled hypertension over the past 20 years and a 40 pack-year history of smoking cigarettes.

On physical examination, blood pressure was noted at 182/100 mm Hg, heart rate 87 beats per minute, respiratory rate 15 breaths per minute, and oxygen saturation 98% on room air. The patient was afebrile. Head, neck, pulmonary, abdominal, and back examinations were unremarkable. CV examination revealed normal heart sounds without murmurs. Normal and equal peripheral pulses were palpable in the upper and lower extremities.

Management Course

The patient was given an aspirin and sublingual nitroglycerin without improvement. Morphine sulfate provided some relief. His ECG showed normal sinus rhythm and nonspecific ST changes. Chest radiograph was negative for pneumothorax and showed a normal appearing mediastinum. Laboratory studies, including the initial cardiac enzyme, were unremarkable. The patient was considered to have nonspecific but concerning chest pain and plans were made for observation unit admission, serial cardiac enzymes, cardiac monitoring, and further cardiac workup. As part of a routine chest pain evaluation, the emergency physician performed bedside echocardiography and noted a dilated aortic root with a diameter of 4.2 cm (Figure 6-89). Contrast-enhanced CT of the thoracic aorta confirmed suspicions of a proximal aortic dissection. CV surgery was emergently consulted and a timely repair was performed without incident.

Commentary

Case 2 exemplifies the utility of routine bedside echocardiography by emergency physicians during the evaluation of nonspecific chest pain. This patient's aortic dissection may have caused a myocardial infarction, aortic valve failure, cardiac tamponade, or death had it not been identified in the ED. Patients with aortic dissection often present without classic symptoms or physical findings. Bedside echocardiography performed by emergency physicians can provide essential information to help expedite disposition and treatment.

Case 3

Patient Presentation

A 30-year-old pregnant woman, 31-weeks gestational age, presented to the ED with 1 day of severe shortness of breath. This was her first pregnancy and she had regular prenatal care and an uncomplicated course. She was a recent immigrant from East Africa and reported no significant past medical history. She had mild swelling of her ankles, which was unchanged during the past few months. On physical examination, blood pressure was 105/60 mm Hg, heart rate 96 beats per minute, respiratory rate 20 breaths per minute, temperature 97°F, and oxygen saturation 97% on room air. The patient was in no distress. Abdominal exam revealed a gravid uterus consistent with the stated gestational age. Pulmonary exam revealed diffuse wheezes. There was no murmur appreciated on the initial cardiac examination. There was no appreciable jugular venous distension and minimal ankle edema.

Management Course

Initially she was thought to have reactive airway disease and given a nebulized albuterol treatment without improvement. There was concern for PE given the patient's severe symptoms and gestational status. ECG showed a normal sinus rhythm at 95 beats per minute with a small R wave in lead V1. Cardiac enzymes were in the normal range, but the patient's chest radiograph showed pulmonary edema (Figure 6-90A). The tentative diagnosis was peripartum cardiomyopathy. Bedside echocardiography was performed by the emergency physician and showed normal left ventricular size and function, significant LAE, and obvious severe mitral stenosis (Figure 6-90B). Even after the diagnosis was established, a murmur could not be appreciated by several staff physicians. The patient was admitted to the intensive care unit (ICU) and had a cesarean section delivery the next day.

Commentary

This case shows the utility of point-of-care cardiac ultrasound for patients with undifferentiated shortness of breath and to determine the underlying etiology in patients with pulmonary edema. This patient had no past medical history, but emigrated from east Africa, where rheumatic valve disease is common. Also, she was in the third trimester of pregnancy and patients with significant mitral stenosis often experience hemodynamic deterioration during the third trimester or during labor and delivery. Additional displacement of blood volume into the systemic circulation during contractions makes labor particularly hazardous; therefore the patient had optimal medical management and early delivery via cesarean section. As is common in emergent settings, no murmur could be appreciated because the patient was in significant distress and had a rapid respiratory rate with expiratory wheezes. This case demonstrates the significant limitations of the stethoscope and other parts of the physical exam, and highlights the utility of point-of-care cardiac ultrasound in patients with severe valve disease.

The authors thank Ben Dolan, MD and Sanjay Vasudeva, MD for their contributions to this chapter.