Use of point-of-care ultrasound in the management of patients presenting with shock: the treatment implications of an early bedside diagnosis of pulmonary embolism

Abstract

Point-of-care ultrasound has been used to identify real-time indicators of acute obstruction to right ventricular outflow and aid appropriate diagnosis and management of patients presenting with extensive pulmonary embolism in whom haemodynamic instability permits only bedside investigation. We present the case of a 70-year-old woman who presented with shock. A focused bedside echocardiography was performed and showed left ventricular septal wall flattening and a severely dilated right ventricle with impaired systolic function. The right atrium was dilated with a floating thrombus visible on the sub-xiphoid view. The patient was treated with intravenous systemic thrombolysis (alteplase) prior to undergoing CT pulmonary angiogram. This showed saddle pulmonary embolus, with extensive thrombus in the main and all lobar pulmonary arteries bilaterally, with evidence of right heart strain.

Background

Identifying the cause of shock can be difficult in the absence of advanced imaging. However, patients who remain clinically unstable with sustained hypotension are not able to be safely transported for these investigations. Point-of-care echocardiography in these circumstances has been shown to be a valuable tool for both diagnosis and prognostication.¹

Case presentation

A 70-year-old woman was brought in by ambulance to a district general hospital following an episode of exertional dyspnoea followed by collapse. She had led a remarkably healthy lifestyle and was not on any regular medication. On arrival, she had a patent airway and was conversing but was in extreme shock with a sustained systolic blood pressure of 30 mm Hg. She was tachycardic, had a Glasgow Coma Scale of 15, temperature of 36.4°C and a glucose level of 5.9 mmol/L.

Initial resuscitation started with intravenous fluid (Hartmann’s solution), but was escalated to metaraminol, a peripherally administered vasopressor when her blood pressure remained consistently low despite 2 L of fluid. An ECG and bedside echocardiography were performed.

Investigations

Her ECG showed S₁Q₃T₃ (figure 1). The focused bedside echocardiography performed showed left ventricular septal wall flattening with impaired left ventricular systolic function and a severely dilated right ventricle (video 1). The right atrium was dilated with a floating thrombus visible on the subcostal view (video 2).

Figure 1.

ECG showing S₁Q₃T₃ pattern.

Video 1.

Download video file ^{(1.1MB, mp4)}

DOI: 10.1136/bcr-2019-233670.video01

Video 2.

Download video file ^{(1.4MB, mp4)}

DOI: 10.1136/bcr-2019-233670.video02

Treatment

A central venous catheter and an arterial line were placed to facilitate norepinephrine infusion, as she had reached maximum permitted infusion rate of metaraminol (10 mg/hour) with minimal effect to the patient’s blood pressure. She was then given systemic thrombolytic therapy (10 mg bolus of alteplase followed by an infusion of 90 mg over 2 hours) and completed this prior to undergoing CT pulmonary angiogram.² This showed saddle pulmonary embolus, with extensive thrombus in the main and all lobar pulmonary arteries bilaterally, with evidence of right heart strain (right ventricular enlargement, flattening of the interventricular septum and inferior vena caval contrast reflux). There was also heterogeneous low attenuation in the posterior aspect of the right atrium that could represent the thrombus visualised on bedside echocardiography. She underwent same day Ekosonic Endovascular System (EKOS) for its ability to deliver a targeted dose of thrombolysis to the pulmonary arteries. EKOS differs from catheter-directed thrombolysis as it utilises a high-frequency ultrasound to enhance penetration of thrombolytic therapy into selective targets and lowers the overall systemic dose of the thrombolytic agent, theoretically reducing the risk of bleeding.^{3 4}

Left and right catheters were positioned without complication. Peak pulmonary arterial pressure was measured at 32/8 mm Hg with a mean of 17 mm Hg (normal pulmonary arterial pressures are 15–30 mm Hg systolic and 4–12 mm Hg diastolic). There was good immediate response with peripheral blood pressure increasing to 130 mm Hg systolic (from 80 to 90 mm Hg systolic).

Outcome and follow-up

She was later found to have terminal gastric carcinoma, which was the likely precipitant of the pulmonary embolism. She remained an inpatient for 2 weeks, before being discharged home with subcutaneous daily low molecular weight heparin injections. She remained well and lived for another 9 months.

Discussion

This patient presented to the emergency department with obstructive shock. Obstruction of the great vessels of the heart characterises this phenomenon and may be caused by cardiac tamponade, constrictive pericarditis, aortic stenosis, tension pneumothorax and extensive pulmonary embolism. In all of these circumstances, an increasing right ventricular afterload, wall tension and hence oxygen demand leads to right ventricular ischaemia and reduced contractility. This in turn leads to a reduction in left ventricular preload, decreased cardiac output and a reduction in right ventricular coronary perfusion pressure. Obstructive shock and rapid deterioration to death is inevitable in the absence of time critical intervention.⁵

In a study of patients diagnosed with pulmonary embolism, Petruzzelli et al showed that a range of ECG abnormalities could present with ST depression and tachycardia being the most common findings (50% and 44%, respectively). S₁Q₃T₃ pattern was seen in 16% of patients. This is defined as an S wave in lead I and Q wave in lead III, each of amplitude greater than 1.5 mm, and a T wave inversion in lead III.⁶

Point-of-care ultrasound has been used to identify real-time indicators of acute obstruction to right ventricular outflow and aid appropriate diagnosis and management of patients presenting with extensive pulmonary embolism in whom haemodynamic instability permits only bedside investigation. Point-of-care echocardiography has been shown to be a valuable tool for both diagnosis and prognostication in these circumstances.^{7 8} Abbasi et al described the use of bedside ultrasound to reveal extensive thromboses in the left femoral vein and left popliteal vein in a patient with unstable vital signs.¹ In the case of pulmonary embolism, point-of-care ultrasound may identify right ventricular strain, dysfunction and dilatation. McConnell’s sign of right ventricular dysfunction with preserved apical function is another common finding in the setting of pulmonary embolism.⁹ Studies have indicated that when point-of-care ultrasound was performed by emergency physicians, identifying right ventricular dilatation had a sensitivity of 90% and specificity of 26% for detecting pulmonary embolism.¹⁰ Where point-of-care ultrasound is used in haemodynamically unstable patients, the absence of the aforementioned signs can be used to redirect focus towards other causes. Where patients present without haemodynamic instability, point-of-care ultrasound has a low negative predictive value and CT pulmonary angiogram remains the gold-standard investigation.¹¹

Learning points.

• Point-of-care ultrasound is useful in characterising and diagnosing shock in the undifferentiated patient.

• A range of ECG abnormalities could present in patients with pulmonary embolus, with ST depression and tachycardia being the most common findings.

• Obstructive shock can be caused by cardiac tamponade, constrictive pericarditis, aortic stenosis, tension pneumothorax and extensive pulmonary embolism.