Abstract
Echocardiography can play a key role in emergency situations such as complications of myocardial infarction, pericardial tamponade, aortic dissection, pulmonary embolus, and trauma is discussed. Key echocardiographic findings, significance, and clinical implications as well as the use of cardiac ultrasound in code situations and assessing shock are covered.
Keywords
aortic dissection, cardiac trauma, complications of myocardial infarct, echocardiographic emergencies, shock, tamponade
Introduction
Echocardiography can be used appropriately to diagnose and triage emergent situations. The life-threatening pathologies in which real-time assessment by echocardiography can be critical include pericardial tamponade, aortic dissection, acute myocardial infarction (MI), acute pulmonary embolus (PE), and cardiac trauma. These conditions may cause severe chest pain, dyspnea with hypoxia, hypotension, and ultimately cardiogenic and respiratory shock. Even in cases where the primary cause of a patient’s deteriorating condition is unclear, such as isolated profound hypotension, the importance of echocardiography in rapidly assessing heart function and ruling out these critical abnormalities in an unstable patient cannot be understated.
This chapter is intended to be a guide to echocardiography in the acute scenario, that is, “echo on-call,” or “STAT” requests. In these situations, the sonographer must quickly grasp (1) the clinical scenario, (2) the indication for the exam, that is, the specific question being asked, and (3) key pathologies that must be ruled in or out. If a specific pathology is found, the ensuing clinical management decisions may be beyond the scope of the specific sonographer and this text, but they are touched upon in the interests of facilitating rapid patient care.
Cardiovascular Emergencies
Cardiogenic shock is heralded by profound hypotension and often respiratory failure. Specifically, systolic blood pressure falls below 80 mm Hg, with signs of end-organ insufficiency (cool extremities, altered mentation) and there is dyspnea, tachypnea, and hypoxia. This is a common and compelling scenario for emergency echocardiography.
From the broadest perspective, there are four very common acute life-threatening emergencies in which echocardiography may assist with diagnosis and/or triage: MI (and its related complications), tamponade, aortic dissection, and PE . Each has specific clinical settings, signs, and symptoms that would lead a clinician to suspect their occurrence in a given patient; although the sonographer may assess for echocardiographic signs of all in one exam, it is best to have an idea of the most likely suspected condition(s) to hasten the relevant imaging and patient care.
Acute MI and mechanical complications of MI are discussed fully in Chapter 18 , Chapter 19 . For rapid reference, the most salient echocardiographic diagnoses are reproduced here in Table 13.1 . To be clear, in a patient who clearly has acute symptoms of myocardial infarct and ST elevations on electrocardiogram (ECG), coronary angiography and urgent revascularization is the first-line treatment, and obtaining an echocardiogram to confirm wall motion abnormalities would only be an impediment to appropriate treatment. Once the patient is stabilized or revascularized, if acute decompensation occurs, the key findings to assess on echocardiography are detailed below.
| Mechanical | Other Causes | |
|---|---|---|
| Complications of MI | Acute MR (ruptured papillary muscle | Global LV failure |
| VSD | RV failure/RV infarct | |
| Pseudoaneurysm Free wall rupture Hemopericardium and tamponade | LVOT obstruction | |
| Tamponade | LV rupture or RV puncture Postcardiac surgery Aortic dissection | Pericarditis Malignant Renal |
| Aortic dissection | Traumatic (recent instrumentation, deceleration injury) | Spontaneous Aortic aneurysm |
| Pulmonary embolus |
Note that these mechanical complications tend to occur 5–14 days after the actual coronary artery occlusion. All represent varying degrees of tissue necrosis, of papillary muscle versus ventricular wall, due to hypoxia. They typically occur in patients who have had large infarcts, or delayed or unsuccessful revascularization. The mortality rate of all is high and depends on rapid identification, stabilization, and repair.
Acute Mitral Regurgitation (Flail Leaflet) ( Fig. 13.1 , 
)
Mitral regurgitation (MR) may occur both acutely and chronically in patients with MI. When there is sudden hypotension and respiratory distress in the days after a large MI, one potential cause could be rupture of the papillary muscle trunk, tip, or chordae causing acute severe MR.
. To assess for flail mitral valve:
- 1.
Obtain a standard parasternal long-axis view showing the mitral valve. Ask:
Do the mitral valve leaflet tips meet normally (i.e., touch each other just below the annulus)?
Or does the tip of one prolapse or “flail” back into the left atrium in systole? (see Fig. 13.1 and
)
- 2.
Place a color Doppler sector over the mitral valve and left atrium. Ask:
Is there a jet of MR (high velocity or turbulent speckled flow in systole)? In many cases, this will be directed eccentrically towards either the anterior or the posterior wall of the left atrium. Typically, a flail leaflet will direct the MR jet away, that is, in the opposite direction, from the damaged leaflet itself (refer to Fig. 19.2 ; see
).
- 3.
Repeat two-dimensional (2D) imaging and color Doppler scans of the mitral valve in apical four-chamber and apical three-chamber windows. For technical reasons, it is not unusual for poor image quality to preclude an absolute determination of whether there is a flail leaflet or not, but an eccentric jet of brisk MR or a chordal structure oscillating in the left atrium proximal to the mitral valve (
) raises the strong possibility of ruptured mitral apparatus.
The figures in this chapter show an example of posterior mitral leaflet flail. Examples of anterior mitral leaflet flail are shown in Chapter 19 , Figs. 19.1 and 19.3, and
.
Urgent management: Even the suspicion of flail mitral leaflet should generally trigger immediate cardiac surgical consultation. If needed, a transesophageal echocardiography (TEE) may be performed in the operating room (OR), or if the patient is in an intensive care unit with ventilator and pressor support providing enough stabilization, bedside TEE may be considered to confirm or refute the diagnosis. Pressors and an intraaortic balloon pump (IABP) may allow enough stabilization preoperatively to get the patient to the operating room.
Ventricular Septal Defect
Another cause of sudden hypotension and pulmonary edema in a patient in the peri- and post-MI period is rupture of the interventricular septum. This causes oxygenated blood to flow from the left to the right ventricle and mix with deoxygenated blood. Ventricular Septal Defects (VSDs) may occur in the anteroseptum (best seen in parasternal windows) due to anterior MIs or in the inferoseptum (best seen in apical four-chamber and subcostal windows) as a result of inferior MIs. Both types of VSDs may be screened for using parasternal short-axis windows. Using color Doppler is essential to detecting these ruptures, because the tissue discontinuity is often slit-like or serpentine and may not be readily visible on 2D imaging alone.
To assess for VSD:
- 1.
Obtain a standard parasternal long-axis view showing the left ventricle (LV) and right ventricle (RV). Ask:
Is the interventricular septum of normal thickness and contracting during systole?
- 2.
Place a color Doppler window over the interventricular septum, particularly any akinetic sections or segments with echo drop-out.
- •
Color flow from left to right penetrating through the septum indicates a VSD. (See Chapter 19 , Fig. 19.4 A and
.)
- •
Place a continuous wave (CW) Doppler cursor line through the color flow. If one measures the peak velocity of the CW Doppler flow envelope, the interventricular pressure gradient (Δ P ) = 4 × peak gradient (where peak gradient is expressed in m/s) ( Fig. 13.2B ; see also Fig. 13.3E , later).
FIG. 13.2
Ventricular septal defect.
(A) The left panel shows a discrete area of echo dropout in the mid-inferior septum. The right panel with color Doppler demonstrates left-to-right flow through a large muscular VSD. (B) Flow velocities by PW Doppler are relatively low (<1.0 m/s), which is consistent with a large defect. The patient had suffered an IMI 2 weeks ago; at which time, cardiac angiography revealed totally occluded vein grafts to his right coronary artery.
FIG. 13.3
Stab wound VSD.
Transthoracic views on 2D (A and B) and color Doppler (C and D) of a VSD caused by knife attack in parasternal long-axis (A and C) and short-axis (B and D) views. E shows the calculation of interventricular pressure gradient by Bernoulli equation. The patient ultimately expired from RV rupture and VSD, despite attempts at emergent surgical repair.
- •
The narrower the neck of the color flow and the higher the peak velocity of the flow, the smaller or more restrictive the VSD is.
- •
- 3.
Rotate the transducer clockwise 90 degrees and obtain parasternal short-axis windows of the LV and interventricular septum. Tilt the transducer apically to sweep the imaging plane from base to apex. Look for akinetic areas or focal echo dropout. Turn the color Doppler sector to cover the interventricular septum, and similarly sweep from base to apex looking for color flow from left-to-right. (See Chapter 19 , Fig. 19.4 B and
.)
- 4.
In apical four-chamber view, examine the interventricular septum on 2D images, then position a color Doppler sector over the septum. Fig. 13.2 and
show an example of an inferoseptal VSD.
- 5.
In subcostal four-chamber view, turn the color Doppler sector on and position it over the interventricular septum. Again, look for color flow through the septum from left to right.
Urgent management: The treatment of choice is early surgical closure, which reduces mortality. Basal septal rupture is technically more difficult to repair fully, in part due to proximity to the mitral valve. In poor operative candidates, percutaneous closure may be considered (shown in
).
Pseudoaneurysm
A pseudoaneurysm, or false aneurysm, is a locally contained rupture of all myocardial layers that is locally contained only by thrombus and pericardial adhesions. They typically have a narrow neck that allows blood flow to communicate freely with the left ventricular cavity and tend to grow and rupture.
To assess for pseudoaneurysm: The most common locations are the basal inferior or inferolateral (for inferior MIs) and apical segments (for anterior MIs). They can vary greatly in size from very small spaces to large fluid collections. (See Chapter 19 , Fig. 19.5 , and 
.) Thus look carefully with 2D imaging:
- 1.
At the LV apex on apical four- and two-chamber windows, and
- 2.
At the basal inferior and inferolateral segments on parasternal and long-axis three- and two-chamber windows for any echo-free space.
- 3.
If any echo-free or inhomogeneously echogenic space is seen, particularly if it appears to be bulging during systole, place a color Doppler sector over the area including the nearby ventricle and look for blood flow from the LV into the space (
).
- 4.
If the diagnosis is still uncertain and patient stable, the use of intravenous (IV) echocardiographic contrast can demonstrate flow into the pseudoaneurysm (see Chapter 19 , Fig. 19.5B , and
).
Urgent management: If echocardiography raises the possibility of pseudoaneurysm, but cannot confirm it or cannot distinguish it from aneurysm, cardiac MRI or LV angiography may be required for definite diagnosis. There is a 30%–45% risk of evolving to complete free wall rupture (below) and amortality rate up to 50%, so urgent surgery to close or patches the rupture is considered the definitive therapy for pseudoaneurysms.
Free Wall Rupture
Complete rupture of the ventricular free wall is typically sudden and catastrophic, and rarely permits time for echocardiography. It may be suspected when acute cardiogenic shock follows a large unreperfused MI, especially if signs of tamponade or electromechanical dissociation are present. Fig. 19.6 and 
show examples of a free wall rupture that rapidly evolved into complete rupture, tamponade with hemopericardium (see next section), and ultimately the demise of the patient. Immediate surgery is the only hope of surviving this with temporizing measures including fluids, inotropes, IABP, and/or peripheral ventricular assist devices utilized if needed to get the patient to surgery.
Nonmechanical Causes of Cardiogenic Shock
If the above mechanical causes for cardiac shock, including tamponade, are not found on echocardiography, then one must consider other potential causes that may contribute, such as the following:
- 1.
LV failure: This is illustrated by poor overall ejection fraction and may represent global hypokinesis, reinfarction, or infarct extension.
- 2.
LV outflow tract obstruction: This is associated with a hyperdynamic base, upper septal hypertrophy and small LV outflow tract, and systolic anterior motion of the mitral valve. If these findings are noted, pulse wave (PW) and CW Doppler of the LV outflow tract should be performed, placing the sample volume at the area of highest velocity in the subaortic area (using the color Doppler window as a guide).
- 3.
RV failure, which may be secondary to RV infarct (virtually always associated with inferior LV infarct and wall motion abnormalities) or PE (see later).
Tamponade
If fluid accumulates in the pericardium at high-enough pressure to impede cardiac filling, the clinical syndrome of hypotension and dyspnea due to decreased cardiac output known as tamponade will result. In the setting of a recent MI, tamponade may occur abruptly from free wall rupture as discussed above. In patients who have had recent coronary angiography and angioplasty, however, one should also consider an iatrogenic complication such as coronary artery dissection. Aortic dissection, either due to recent angiography or other causes (spontaneous, or trauma-induced), is another important cause of tamponade and sanguineous pericardial effusions. Also, patients who have just undergone pacemaker or automated implantable cardiac defibrillator (AICD) placement or RV biopsy are at risk for hemorrhaging into the pericardium. Oncology patients, particularly those with breast, lung, and hematologic malignancies as well as mesothelioma or melanoma, may present acutely or subacutely with a new hemodynamically significant pericardial effusion. Lastly, patients with severe renal failure may also develop significant pericardial effusions, although these do not accumulate rapidly.
Echocardiography is the foremost tool in evaluating for tamponade. The sonographer must rapidly identify the size and distribution of the pericardial effusion, and its hemodynamic impact. Hemodynamically significant effusions will often (1) cause collapse of chambers of the heart, typically the right atrium and ventricle first, and (2) cause respirophasic flow variation in the atrioventricular valves (as well as the corresponding outflow tracts of the left and right heart) in opposing directions, as measured by peak flow velocities.
A quick but comprehensive overall protocol for assessing pericardial effusions is as follows:
- 1.
Place ECG leads (and if time permits, a respirometer; alternatively, use the ECG baseline dial to manually indicate inspiration and expiration).
- 2.
On supine patients, obtain a quick subcostal view to look for any pericardial fluid ( Fig. 13.4 ). Since fluid tends to flow dependently, it often accumulates above the liver and anterior/inferior to the right heart. Fortuitously, this is also the position where a pericardiocentesis needle is targeted towards for drainage.
- •
If fluid is present, begin a full evaluation from this window.
- •
Note location and overall dimensions. In particular, it is useful to note the largest linear dimension (in centimeter), as well as the measurement anterior/inferior to the right heart, for planning future pericardiocentesis or other surgical therapies.
- •
Two-dimensional images of four-chamber view (still subcostal) should be obtained, looking for indentation or collapse of the right atrium and/or RV (as well as left-sided chambers) (
).
- •
Show the inferior vena cava (IVC) over multiple beats ( Fig. 13.4B ): assess for size (>2.1 cm is dilated) and respirophasic size variation (normally the diameter reduces by 50% with inspiration). This will give a rough approximation of right atrial (RA) filling pressure. A dilated IVC that remains plethoric even in inspiration is a sign of markedly elevated central venous pressure that accompanies tamponade greater than 90% of the time.
- •
