Key Points
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Point-of-care ultrasound is a noninvasive, reliable tool to rapidly and accurately assess hemodynamically unstable patients at the bedside.
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Hypovolemic, cardiogenic, obstructive, and distributive shock can be readily differentiated using established point-of-care ultrasound protocols.
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Goal-directed, serial point-of-care ultrasound examinations can be performed to monitor critically ill patients in shock.
In hemodynamically unstable patients, point-of-care ultrasound allows providers to rapidly differentiate the etiology of shock at the bedside and monitor response to therapies. Selecting and delivering life-saving interventions to reverse shock is entirely dependent on identifying the underlying etiology; for example, massive fluid resuscitation required in hypovolemic shock would cause immediate decompensation if delivered to a patient with acute cor pulmonale, or inotropic therapy initiated in a volume-depleted patient could likewise end in death. The majority of point-of-care cardiac ultrasound exams in critically ill shock patients consist of five standard assessments that allow for accurate classification and initiation of appropriate therapy :
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Left ventricular size and function
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2
Right ventricular size and function
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3
Pericardial effusion
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4
Intravascular volume status
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5
Gross valvular abnormalities
Case 22.1
Case Presentation
A 59-year-old man with a history of coronary artery disease and myocardial infarction presented to the emergency department (ED) with lightheadedness and near syncope. Vital signs: temperature 38°C, pulse 122 bpm, blood pressure 86/40 mm Hg, respiratory rate 28 per minute, oxygen saturation 88%.
Physical exam: Lethargic, moderate respiratory distress, dry mucous membranes, unable to complete full sentences, tachycardic without murmur, faint crackles in bilateral bases, no peripheral edema.
Initial testing was significant for leukocytosis, elevated lactate, and pyuria on urinalysis. Chest x-ray revealed bilateral interstitial opacities with an oxygen saturation of 88% on a 100% non-rebreather mask. ECG revealed a left bundle branch block. Initial troponin was normal.
Assessment
Sepsis was suspected as the underlying cause of patient’s hypotension and lethargy based on the presence of fever and pyuria. The chest radiograph was attributed to development of acute respiratory distress syndrome given the patient’s volume depletion without peripheral edema. Intravenous fluid resuscitation was initiated, but neither blood pressure nor clinical exam improved after 2 L of intravenous fluids. The critical care team was consulted and performed a focused cardiac and lung ultrasound exam that revealed the following:
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Left ventricle (LV) size and function: LV dilated with severely reduced function (reduced endocardial excursion, reduced myocardial thickening, and limited septal motion of the anterior leaflet of the mitral valve) ( Fig. 22.1 and
Video 22.1
).
Figure 22.1 Case 22.1—Parasternal Long-Axis View.
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Right ventricle (RV) size and function: Limited assessment, RV seen only in parasternal long-axis view; however, appears mildly enlarged, possibly hypocontractile from this view.
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Inferior vena cava (IVC) size and collapsibility: Dilated to almost 3 cm, noncollapsible ( Fig. 22.2 and
Video 22.2
).
Figure 22.2 Case 22.1—Subcostal Inferior Vena Cava (IVC) View With a Dilated IVC.
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Pericardial effusion: Absent.
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Valvular function: Moderate mitral regurgitation (MR) seen on color flow Doppler ( Fig. 22.3 and
Video 22.3
).
Figure 22.3 Case 22.1—Parasternal Long-Axis View With Color Flow Doppler Revealing Moderate Mitral Regurgitation.
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Lung ultrasound: Anterior lung zones with confluent B-lines with smooth, thin pleura that are sliding ( Fig. 22.4 and
Video 22.4
).
Figure 22.4 Case 22.1—Lung Ultrasound (Upper Lobes) With Confluent B-Lines Bilaterally.
The severely reduced global LV function suggested a possible primary cardiac cause of hypoperfusion. The bilateral anterior lung zones with confluent B-lines and a smooth, thin, sliding pleural line is consistent with hydrostatic pulmonary edema with a pulmonary artery occlusion pressure greater than 18 mm Hg. The dilated IVC provides further evidence of elevated cardiac filling pressures. Absence of severe MR confirmed acute cardiogenic shock from LV failure as the primary cause. Dobutamine infusion, diuresis, and anticoagulation were initiated with improvement in dyspnea, urine output, and mental status. Repeat troponin was elevated, and urgent cardiac angiography revealed an occluded left anterior descending artery that was treated with angioplasty and stent placement.
Case Resolution
Cardiogenic shock presents with signs of a low cardiac output, usually oliguria, cool extremities, decreased mental status, and hydrostatic pulmonary edema. Patients without a history of congestive heart failure warrant further investigation for an acute inciting event. The treatment of cardiogenic shock should be directed at reversing the underlying cause, most commonly ischemia, infarction, or acute on chronic LV failure. Diuretic and/or inotropic therapy with dobutamine should be initiated to support perfusion. Response to therapy can be confirmed and monitored noninvasively with serial repeat bedside ultrasound exams to assess LV systolic function and interstitial pulmonary edema.
Case Pearls
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The presence of bilateral B-lines over the anterior and lateral lung zones and a thin, smooth, sliding pleura are diagnostic of hydrostatic pulmonary edema.
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Screening of the mitral valve for severe MR with color flow Doppler should be performed in any patient with hydrostatic pulmonary edema and shock.
Case 22.2
Case Presentation
A 43-year-old woman with a history of asthma and recent ankle surgery presented to the emergency department (ED) with progressively worsening dyspnea over the prior 2 weeks, noting a lack of response to the new bronchodilators that were prescribed by her doctor. Vital signs: pulse 130 bpm, blood pressure 80/42 mm Hg, respiratory rate 30 per minute, oxygen saturation 94% on a non-rebreather mask.
Physical exam: Patient appeared fatigued, slightly lethargic with mildly labored breathing. Her lungs were clear anteriorly with an occasional faint wheeze heard posteriorly. The remainder of the physical exam was normal with the exception of left leg edema distal to the calf.
Initial testing with arterial blood gas revealed severe hypoxemia with a mild respiratory alkalosis. Chest x-ray was normal.
Assessment
Based on her severe hypoxemia and normal chest x-ray, an acute pulmonary embolism (PE) as the cause of her shock and respiratory distress was strongly suspected. While awaiting a computed tomography (CT) angiogram of the chest, a bedside ultrasound exam was performed to investigate the cause of her respiratory failure. During the ultrasound examination, her blood pressure dropped, leading to cardiac arrest. Bedside ultrasound exam revealed the following:
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Left ventricle (LV) size and function: Hyperdynamic function with a “ D ”-shaped septum on parasternal short-axis views, consistent with acute cor pulmonale with underfilling of LV ( Fig. 22.5 and
Video 22.5
).
Figure 22.5 Case 22.2—Parasternal Short-Axis View With a Dilated Right Ventricle and “ D ”-Shaped Septum.
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Right ventricle (RV) size and function: Severely dilated RV noted in both apical 4-chamber and parasternal short-axis views. Apex of heart is dominated by the RV and is contracting well, despite the akinesis of the RV free wall (McConnell’s sign) ( Fig. 22.6 and
Video 22.6
).
Figure 22.6 Case 22.2—Apical 4-Chamber View Reveals a Dilated Right Ventricle.
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Inferior vena cava (IVC) size and collapsibility: Diameter dilated to almost 3 cm, noncollapsible.
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Pericardial effusion: No effusion is seen in any view.
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Valvular function: Valve structure is grossly normal; color flow Doppler revealed no appreciable mitral regurgitation (MR).
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Lung ultrasound: Lung ultrasound showed a predominant A-line pattern with visible lung sliding seen over both anterior chest walls ( Fig. 22.7 and
Video 22.7
).
Figure 22.7 Case 22.2—Lung Ultrasound (Upper Lobes) With A-Lines Bilaterally.
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Lower extremity compression ultrasound exam for deep venous thrombosis (DVT): Visible echogenic thrombus is seen within the common femoral vein consistent with presence of DVT ( Fig. 22.8 and
Video 22.8
)
Figure 22.8 Case 22.2—Right Lower Extremity Ultrasound of the Femoral Vein Shows Echogenic Thrombus in the Vein.
The normal aeration pattern throughout both lungs excluded any interstitial process as the cause of dyspnea. Bilateral A-line pattern with normal lung sliding in a patient with acute respiratory failure narrows the differential diagnosis to two main possibilities: obstructive airway disease (asthma/chronic obstructive pulmonary disease) or PE. This patient had risk factors for both asthma and PE. The cardiac ultrasound exam revealed a dilated RV with septal bowing producing a D-shaped LV indicative of combined volume and pressure overload of the right heart, or cor pulmonale. Acute pressure overload results in RV enlargement with a relatively thin RV wall, normally measuring <5 mm in thickness. Chronic RV pressure strain causes RV hypertrophy, often with RV wall thickness >1 cm. This patient had a dilated RV with a thin wall suggesting an acute process. The apical 4-chamber (A4C) view shows the apex is primarily formed by the RV, a highly abnormal finding, which is further evidence of acute RV pressure overload. Furthermore, the RV apex is contracting well, whereas the midchamber RV free wall is akinetic (McConnell’s sign)—an indicator of RV pressure overload that is strongly associated with acute PE, as well as RV infarction.
Lower extremity compression ultrasound exam was a supplementary exam in this patient with high suspicion of PE. The right common femoral vein had partially occlusive echogenic material within the vein, diagnostic of thrombus.
Case Resolution
Based on her clinical history and point-of-care ultrasound findings, she was presumptively diagnosed with an acute PE. Cardiopulmonary resuscitation was initiated with infusion of tissue plasminogen activator (t-PA). A return of spontaneous circulation was documented within 4 to 5 minutes of initiating resuscitation.
Case Pearls
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A-lines are seen when air is just below the parietal pleura (as in pneumothorax) or deep to the visceral pleura (normal aeration pattern). The location of air is deduced by lung sliding presence (normal aeration) or absence (pneumothorax).
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Acute right heart pressure overload results in RV dilation with a relatively thin RV free wall, normally measuring <5 mm in thickness. Chronic RV pressure overload results in increased RV wall thickness that is often >1 cm.
Case 22.3
Case Presentation
A 49-year-old man with an implanted cardiac defibrillator placed for an unexplained cardiac arrest 10 years earlier presented to the emergency department (ED) with weakness, malaise, and dyspnea developing over 3 days. The patient reported participating in a weekend hiking trip 2 weeks ago.
Vitals signs: temperature 37.7°C, pulse 150 to 160 bpm, blood pressure 88/40 mm Hg, respiratory rate 30 per minute, oxygen saturation 92% on a non-rebreather mask.
Physical exam: The patient was slightly diaphoretic with labored breathing. Breath sounds were coarse bilaterally. Tachycardia with a systolic murmur loudest at the apex was noted. His lower extremities showed no signs of edema or cyanosis. A few scratches were noted on his legs, and the extremities were cool to touch.
Initial testing began with an electrocardiogram revealing supraventricular tachycardia (SVT) without ischemic changes. Portable chest x-ray suggested mild pulmonary vascular congestion without pleural effusions or opacities. Electrolytes and blood gas analysis revealed an acute lactic acidosis, and his white blood count was mildly elevated at 11,400.
Assessment
Based on his low blood pressure, SVT, leukocytosis, and low-grade temperature, sepsis was suspected. He was given an infusion of 3 L of intravenous fluid. Only a minimal response was observed in his blood pressure (90/60 mm Hg). A bedside ultrasound exam for evaluation of the patient’s shock state was performed:
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Left ventricle (LV) size and function: Hyperdynamic function with end-systolic effacement of LV cavity was seen in all cardiac views ( Figs. 22.9 and 22.10 ;
Videos 22.9
,
22.10
, and
22.11
).
Figure 22.9 Case 22.3—Parasternal Long-Axis View With End-Systolic Effacement of the Left Ventricular Cavity.
Figure 22.10 Case 22.3—Parasternal Short-Axis View With End-Systolic Effacement of the Left Ventricular Cavity.
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Right ventricle (RV) size and function: Normal RV shape and function, no appreciable dilation noted ( Fig. 22.11 ,
Video 22.11
)
Figure 22.11 Case 22.3—Apical 4-Chamber View With Normal Right Ventricular Size and Shape.
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Inferior vena cava (IVC) size and collapsibility: Small IVC with pulsatile variation ( Fig. 22.12 ,
Video 22.12
).
Figure 22.12 Case 22.3—Inferior Vena Cava (IVC) View Shows a Small, Easily Collapsible IVC.



