Critical Care Echocardiography

Etienne J. Couture

Caroline E. Gebhard

Stephan Langevin

André Y. Denault

INTRODUCTION

Critical care ultrasound (CCUS) comprises ultrasound evaluation of the heart, lungs, pleural space, intraabdominal organs, nervous and vascular systems. CCUS is designed to be used as a series of simplified, focused examinations that can quickly rule in or rule out a diagnosis, or guide the practitioner to perform additional investigations or procedures. In this chapter we will concentrate on two of the most common problems in the intensive care unit which are hemodynamic instability and hypoxemia. The use of brain, renal, and vascular ultrasound in altered neurologic status, oligoanuria, and vascular access will not be covered. Interested reader can refer to several references regarding these issues (1,2,3,4,5,6).

A PROPOSED APPROACH TO HEMODYNAMIC INSTABILITY

The general approach to patients with hemodynamic instability should include a brief anamnesis, patient examination incorporating the physical examination, monitor waveform analysis, electrocardiographic changes, and laboratory values. This initial rapid assessment must include simultaneous conventional resuscitation management (Fig. 18.1). Despite the increasing importance of CCUS as a primary diagnostic guidance tool, it is important to acknowledge that CCUS is not replacing any conventional diagnostic imaging tools. There have been several proposed approaches for the use of CCUS in patients with hemodynamic
instability. These include the Focused Cardiac Ultrasound or FOCUS (7), the Focused Assessed Transthoracic Echo or FATE (8), the Focused Assessment with Sonography in Trauma or FAST (9), the Rapid Ultrasound for Shock and Hypotension or RUSH (10), and the Hemodynamic Echocardiography Assessment in Real Time or HEART (11) scan protocols that all emphasize the following three points: (1) The examination is performed at the bedside by the responsible clinician; (2) the dynamic images are correlated with the clinical picture; (3) the examination can be repeated as often as needed to monitor the progress. Though both transthoracic echocardiography (TTE) and basic transesophageal echocardiography (TEE) can be used at the bedside, emphasis will be placed on the use of TTE, as this technique is more widely available to anesthesiologists and critical care physicians.

FIGURE 18.1 General approach to shock. In the presence of shock, a brief focused history and examination of the patient and the monitors is performed. In addition, key laboratory values and an electrocardiogram are obtained. Once hypotension is confirmed and the signs of shock are present, an ABC approach is proposed. If these initial steps do not correct the hemodynamic instability, bedside ultrasound examination should be considered. BP, blood pressure; US, ultrasound; TEE, transesophageal echocardiography. (Reproduced with permission of Taylor and Francis Group, LLC, a division of Informa plc. from Denault et al. (5).)

Most of the previously mentioned approaches are based on obtaining a sequence of images limited to specific organs in order to rule out specific conditions such as free abdominal fluid in a trauma patient. So far, there is no evidence that one approach is superior to the other. In our institution we tend to use a pathophysiologic approach that integrates history, physical findings, labs, and echocardiographic findings in order to identify three specific categories of shock based on the concept of venous return (VR). The detailed explanation of VR is beyond the scope of the chapter and those interested in the topic should review those references (12,13,14,15,16).

In simple terms, shock can be easily approached using the concept of VR popularized by Guyton (17). VR is determined by a pressure gradient that, in a steady state, is equal to cardiac output. The pressure gradient corresponds to the difference between the mean systemic venous pressure (P_ms) in the periphery and the right atrial pressure (P_ra). VR is inversely proportional to the resistance to venous return (R_vr) as described by this equation:

This concept allows to categorize hemodynamic instability from reduced VR and, consequently, reduced cardiac output according to one of the three fundamental mechanisms: (1) reduction in systemic venous pressure, (2) increase in right atrial pressure, and (3) increase in resistance to VR (Table 18.1). The use of this
approach will guide how bedside ultrasound will be used when dealing with a patient with hemodynamic instability or shock. CCUS will simply be used to determine the mechanism of shock initially and then to identify the etiology of the shock state.

TABLE 18.1 Classification of Hemodynamic Instability Using the Concept of Venous Return

Reduced mean systemic venous pressure		Increased right atrial pressure	Increased resistance to venous return
Hemorrhagic/hypovolemic shock External bleeding Internal bleeding Thorax Abdominal Pelvis Long bones Distributive shock Septic Nonseptic Anaphylactic Endocrine: ↓ adrenal or thyroid function Liver failure Neurogenic and neuroaxial blockade Pharmacologic and toxic Post CPR and CPB (postreperfusion) Inflammatory:		Myocardial Systolic dysfunction Diastolic dysfunction Valvular Acute valvular regurgitation Mechanical obstruction Outflow tract obstruction Pulmonary embolism Ventilatory Hypoxemia Hypercapnia	Supradiaphragmatic Cardiac tamponade Pneumothorax Mediastinal tamponade Dynamic hyperinflation (auto-PEEP) Infradiaphragmatic Abdominal compartment syndrome IVC obstruction IVC anastomosis Compressive tumors Restrictive devices
	– Burns – Pancreatitis – Multiple trauma – SIRS
CPB, cardiopulmonary bypass; CPR, cardiopulmonary resuscitation; IVC, inferior vena cava; PEEP, positive end-expiratory pressure; SIRS, systemic inflammatory response syndrome. Reproduced with permission of Taylor and Francis Group, LLC, a division of Informa plc. from Denault et al. (15).

FIGURE 18.2 Inferior vena cava. A: Axial T1-weighted magnetic resonance image of the liver showing different positions of the ultrasound probe that can be used to obtain a longitudinal view of the inferior vena cava (IVC). B-D: The subxiphoid (1), anterior axillary line (2), and posterior axillary line (3) positions using the Vimedix simulator are shown. The subxiphoid view is obtained in the supine patient by positioning the probe in the subcostal region with the probe marker placed toward the head at 12 o’clock. The US plane is directed toward the liver to show a longitudinal view of the IVC. The IVC can be distinguished from the pulsatile aorta by identifying the following criteria: (1) the IVC drains into the right atrium; (2) liver surrounds the IVC; (3) lack of pulsatility of the IVC (unless presence of severe tricuspid regurgitation); and (4) hepatic veins draining into the IVC. (Reproduced with permission of Taylor and Francis Group, LLC, a division of Informa plc. from Denault et al. (5).)

Step #1: Ultrasound Imaging of the Inferior Vena Cava and Abdominal Venous Flow

A rapid starting point to identify possible mechanisms of shock or hemodynamic instability in patients unresponsive to standard care is the examination of the size and respiratory variation of the inferior vena cava (IVC). There are several reasons why we start with the IVC: first, ultrasound interrogation of the IVC is classically performed using a subxiphoid view. In some patients, the presence of chest tubes or dressings may prevent access to this view. Since the distal portion of the IVC is intrahepatic and the liver is large, imaging through the liver from any lower right intercostal position can provide an acoustic window to the IVC with a very high success rate (Fig. 18.2) (16,18). Second, it determines the type of shock, if the IVC is small and collapsible reduced mean systemic venous pressure is more likely, cardiogenic shock is unlikely. Third, IVC collapsibility is the best predictor of hypotension before the induction of anesthesia (19). Fourth, it can be used to rapidly estimated right atrial pressure (20,21) and fluid responsiveness (22,23). Finally, from the same acoustic window, it is possible to interrogate the hepatic venous and portal flow and to confirm precisely the mechanism of shock (Fig. 18.3) (24,25).

There are, however, limitations to the use of the IVC to estimate mean systemic venous pressure (20) (Table 18.2). As opposed to spontaneously breathing patients, individuals receiving positive pressure ventilation demonstrate an increase in IVC diameter during inspiration from increased intrathoracic pressure and a decrease in size during expiration. Increased right atrial pressure can be reflected by IVC
size and respiratory variation (20,21). This can be easily demonstrated using M-mode imaging. A recent study on IVC measurement has shown that the use of both transverse and longitudinal assessment of IVC provides better estimation of central venous pressure (21). Finally, dynamic testing such as leg raising and fluid challenge remain the examination of choice in determining preload responsiveness or if there is any benefit in increasing the mean venous systemic pressure in order to improve VR or cardiac output (26,27).

FIGURE 18.3 Shock mechanism. Algorithm to determine shock mechanism using inferior vena cava (IVC) size, respiratory variation during spontaneous ventilation, and hepatic venous flow. (1) In patients with reduced mean systemic venous pressure (P_ms), the IVC is small (<21 mm) with respiratory variation (>50%), and the hepatic venous flow is typically normal or increased due to the reduced dimension of the hepatic vein. (2) In patients with increased resistance to venous return (R_vr), the IVC can be collapsed from an abdominal compartment syndrome or (3) distended from a mechanical obstruction at the junction of the IVC and right atrium (RA) or tamponade. The hepatic venous flow signal will be significantly reduced, monophasic, or absent in both situations. (4) In a situation where the right atrial pressure is increased, the IVC is dilated (>21 mm) without respiratory variation (<50%), and the HFV will be abnormal with reduced systolic (S) to diastolic (D) velocity ratio. AR, atrial reversal hepatic venous flow velocity; D, diastolic hepatic venous flow velocity; HV, hepatic vein; IVC, inferior vena cava; S, systolic hepatic venous flow velocity. (Adapted from (24) and reproduced with permission of Taylor and Francis Group, LLC, a division of Informa plc. from Denault et al. (5).)

In summary, if an unstable patient presents with a small collapsible IVC and fluid responsiveness is present, reduced mean systemic venous pressure will be suspected. Two potential mechanisms will be either vasodilatation as in septic shock or reduction in blood volume such as in hemorrhagic shock. In those patients the aspect of the hepatic and portal venous flow will be normal. CCUS in those patients will then focus on determining the etiology by examination of the thoracic cavity and the abdomen.

TABLE 18.2 Limitations to Using the IVC to Estimate Mean Systemic Venous Pressure

Mechanical obstruction:
	Prominent Eustachian valve, web, tissue, tumor, thrombus, aortic aneurysm, foreign bodies such as filters present in the IVC, narrowing of the IVC right atrial junction
Others:
	Athletic training, large body surface area, mechanical ventilation
IVC, inferior vena cava. Adapted from Beigel et al. (20).

If a large IVC is present then a suspicion of increased right atrial pressure and cardiogenic shock will be raised. Typically, those patients will have an abnormal hepatic and portal venous flow if right heart dysfunction is present (3,24). CCUS will focus on determining the etiology through the cardiac examination.

Finally, resistance to VR occurs in situations where the heart is normal and the blood volume is preserved but the volume cannot get to the heart. It can be above the diaphragm such as tension pneumothorax or tamponade and the IVC will be distended, or below the diaphragm as in abdominal compartment syndrome and the IVC will be small. In such a situation hepatic and portal venous flows are abnormal or absent (16,24). The size of the IVC will determine the etiology and CCUS will then focus either on the thoracic or abdominal compartment.

Step #2: CCUS in Patients With Reduced Mean Systemic Venous Pressure

In spontaneously breathing patients, reduced mean systemic venous pressure is typically associated with a small IVC that varies in dimensions with respiration. Another useful echocardiographic feature to evaluate mean systemic venous pressure is to interrogate the hepatic venous flow using pulsed wave Doppler. The normal hepatic venous flow generates a triphasic Doppler waveform that corresponds to the right atrial waveform (Fig. 18.3). Reduced mean systemic venous pressure is typically associated with normal hepatic venous flow. In certain cases of reduced mean systemic venous pressure, the hepatic venous flow velocity can be increased because the hepatic vein is smaller in size, and consequently, blood flow velocity is higher in this smaller vessel.

Once reduced mean systemic venous pressure is identified as a mechanism of hemodynamic instability, the next step is to identify its etiology. Two most likely causes are vasodilatation such as septic shock and reduced circulatory blood volume such as during hemorrhagic shock. There are several ways to distinguish one from the other: patient with hemorrhagic shock are typically cold and clammy as opposed to those with septic shock who are warm. Point-of-care or noninvasive measurement of hemoglobin can quickly distinguish between the two, although in acute hemorrhage, hematocrit values may remain normal for a while because the associated reduced plasma volume is paired with a reduction in red blood cells. Invasive or noninvasive oximetry will typically be reduced in hemorrhagic shock but remain normal in vasodilatory shock (28,29).

Blood loss can be external or internal including bleeding sources from the thorax (Fig. 18.4A), peritoneal cavity (Fig. 18.5), retroperitoneal cavity, pelvis, long bones, or gastrointestinal tract. Identification of a hemothorax and free fluid in the abdomen can be easily achieved with CCUS. If blood loss is not the cause of the reduced mean systemic venous pressure, a distributive shock is to be considered. Septic condition needs to be ruled out by clinical and laboratory examination. Limited TTE views of the heart may show large vegetation. Complex pulmonary effusion (Fig. 18.4B) or lung consolidation associated with pneumonia (Fig. 18.4C,D) can be visualized with CCUS. The diagnosis of a liver abscess, cholecystitis, or pyelonephritis requires skills not covered by CCUS. Also, CCUS is of limited utility in some conditions associated with distributive shock such as anaphylactic shock, pharmacologic central blockade, and Addisonian crisis.

Echocardiography may help distinguish between hypovolemia and vasodilatation. In hypovolemia, the ventricles typically have a small end-diastolic and end-systolic dimension with normal ejection fraction. In a patient with vasodilatation, the end-diastolic size will be normal with a reduced end-systolic size representing an increased ejection of blood against lower afterload. This distinction may be difficult to make in a patient with rapidly changing hemodynamic states, or when both conditions are present simultaneously, particularly in those in whom the baseline end-diastolic volume is unknown.

Step #3: CCUS in Patients With Raised Right Atrial Pressure

In patients with elevated right atrial pressure and shock, a focused goal-directed bedside ultrasound examination must include views to assess the heart. Views are named first based on probe position, namely parasternal, apical, and subcostal views and second by the axis (e.g., long and short) or chambers views (e.g., four-chamber, two-chamber) (Fig. 18.6) (18).

Parasternal Long- and Short-Axis View

The parasternal window is found immediately adjacent to the sternum, in the third or fourth intercostal space. Images obtained in this window are greatly improved by left lateral decubitus positioning, which
moves the heart closer to the chest wall. The parasternal long-axis view (Fig. 18.6A,B) provides images of the aortic and mitral valves, the left atrium and ventricle, and a small portion of the right ventricular outflow tract (RVOT). The septum and inferior walls of the left ventricle (LV) are seen in this view

(Video 18.6A). By rotating the probe 90° clockwise, the parasternal short axis is imaged (Fig. 18.6C,D). Views at the level of the papillary muscles allow for evaluation of LV and RV chamber size and wall motion abnormalities at the midventricular level. Cephalic tilting or steering of the probe allows progressive visualization of the basal segments, mitral valve, aortic valve, and pulmonary arteries. Caudal tilting from the midventricular level allows visualization of the apical segments and the apex

(Video 18.4B).

FIGURE 18.4 Reduced systemic venous pressure from a pulmonary etiology. A: Imaging of complex pleural effusion (hemothorax) in zone 4 using phased array probe for lung ultrasound. B: Imaging of heterogeneous pleural effusion with multiple septations suggesting an empyema in zone 5 using phased array probe for lung ultrasound. C: Imaging of hepatized lung parenchyma in zone 8 using convex probe for lung ultrasound. D: Normal hepatic parenchyma. (Reproduced with permission of Taylor and Francis Group, LLC, a division of Informa plc. from Denault et al. (5).) See

Video 18.4.

Apical Four- and Two-Chamber View

This window is found at the ventricular apex, identified as the point of maximal impulse, near the anterior axillary line (Fig. 18.6E,F). The apical four-chamber view provides a global picture of all four chambers. Chamber size and ventricular interdependence can be evaluated

(Video 18.6C). Tricuspid and mitral valve color Doppler interrogation to rule out regurgitation or stenosis can be done with this view. With little anterior tilt, the left ventricular outflow tract (LVOT) appears and continuous wave Doppler can be applied to evaluate cardiac output (See Chapter 6). The apical two-chamber is obtained by rotating the transducer 90° counterclockwise from this position. The apical two-chamber allows visualization of the left ventricular anterior and inferior walls.

FIGURE 18.5 Reduced systemic venous pressure from abdominal etiology. Free intra-abdominal fluid shown on the right middle axillary coronal abdominal ultrasound image of a 48-year-old patient with a liver laceration after a car accident. A: Free fluid (yellow dotted line) is seen in the hepatorenal space with (B) corresponding coronal computed tomography scan. C: Free fluid in a patient with ascites and (D) the corresponding Vimedix simulator image. (Reproduced with permission of Taylor and Francis Group, LLC, a division of Informa plc. from Denault et al. (5).) See

Video 18.5.

Subxiphoid Four-Chamber and IVC View

A simple way to obtain a subcostal four-chamber from the subxiphoid-IVC view is to rotate the ultrasound probe clockwise, which is analogous to a TTE apical four-chamber view (Fig. 18.6G,H). This image can be difficult to obtain in patients with midline abdominal incisions or mediastinal chest tubes. During external chest compression, this view allows quick evaluation of tamponade, chamber size quantification, and cardiac activity

(Video 18.6G).