Echocardiography is a procedure that has been used in the critical care setting for a long time. Several working groups from different societies have published guidelines and consensus documents suggesting competencies and training programs [1, 2]. However, its expansion has been limited by the absence of an accredited training. Furthermore, echocardiography is apparently complex and often requires a prolonged training in the cardiovascular imaging unit. Therefore, echocardiography is often limited to specific areas such as perioperative cardiac surgery or lung and liver transplantation.

Its use in the cardiology setting has mainly a diagnosis and prognosis role, focusing mainly in its structural perspective for medium and long-term decision-making. However, in the cardiology setting, it may also be used for functional and hemodynamic monitoring at the bed-side [3, 14,15,16], such as using mitral Doppler inflow patterns to guide diuresis, LVOT VTI to optimize pacing, RV systolic pressure (RVSP) estimation to guide therapy in pulmonary hypertension.

There are several algorithms aiming for guiding in the assessment of hemodynamic shock in critically ill patients, based on echocardiography [4,5,6]. These echocardiographic algorithms focus mainly in its structural perspective and do not offer a clear guide on how to interpret the findings in such a complex clinical context, which often leads to starting unnecessary treatment or support measures.

The aim of this article is to show a simple algorithm based on left ventricle outflow tract (LVOT) velocity–time integral for differential diagnosis in hemodynamic shock proposed by the Spanish Critical Care Ultrasound Network Group. This algorithm is based on LVOT velocity–time integral measurement, giving a more functional perspective to the use of echocardiography in the critical care setting. This functional perspective is based on measuring forward flow, by LVOT velocity–time integral measurement, in the LVOT or right ventricle outflow tract (RVOT), which will allow us to measure variables related to perfusion (preload, afterload and contractility). This variable integrated into clinical context may have a potential role in the differential diagnosis for hemodynamic shock in critically ill patients (Fig. 1).

Principles of functional echocardiography

Assessment of hemodynamic status is based on two concepts: perfusion and congestion. Congestion may be assessed by lung ultrasound as well as, hepatic, portal vein and venous renal congestion (VEXUS Score) along with trans-mitral inflow and E/e’ ratio to estimate LV filling pressures. However, in our article, we will focus on perfusion parameters rather than congestion.

Our review will be centered on transthoracic echocardiography, although it might also be used by transesophageal echocardiography.

Written informed consent was obtained from the patients for publication of this case report.

A case series of 4 patients is reported to whom the algorithm based on VTI was performed and its use was crucial for the differential diagnosis and management of the hemodynamic shock.

This is a 73-year-old patient with a medical history of diabetes mellitus on insulin, hypertension and dilated ischemic heart disease (IHD) with left ventricle ejection fraction (LVEF) of 25–30% on diuretic treatment undergoing urgent cholecystectomy for acute cholecystitis. After anesthesia induction a profound hypotension (BP 60/30) and tachycardia (HR 100 bpm) refractory to volume and low-dose administration of ephedrine, is presented. It was decided to do an urgent echocardiography. From the structural perspective, a severe left ventricular systolic function impairment is observed in the echocardiography.

Step 1: What is the cause of this hemodynamic shock? According to clinical context and medical history it could be the following: (a) septic shock due to cholecystitis, or (b) cardiogenic shock secondary to an acute ischemic cardiomyopathy, or (c) relative hypovolemia due to diuretics.

Step 2: What treatment would you give? (1) Fluid therapy, with its associated risk of overloading; (2) vasopressors, with its associated risk of lowering cardiac output and worsening hypoperfusion; (3) inotropic drugs, with its associated risk of worsening the clinical state if hypovolemia or IHD is the cause of the shock.

According to structural algorithms, the images showing low LVEF in the TTE would lead to initiation of inotropic support to improve contractility, whereas with the use of echocardiography from the hemodynamic and functional perspective, an adequate forward flow (VTI of 19 cm and cardiac output of 5,9L/min) is shown. As it is a chronic dilated cardiomyopathy with high end-diastolic volumes, an adequate stroke volume was maintained. Inferior vena cava (IVC) diameter was 20 mm with a distensibility of 10%. Mitral-inflow E/A ratio was 1.2.

The VTI of 19 cm, calculated by TTE, helped us in our differential diagnosis, leading us to suggest that the most likely cause of hemodynamic shock was the low vascular resistance due to anesthetic drugs and treating with vasopressors rather than inotropic support or fluids.

A 67-year-old male patient was admitted to ICU for a post-operative shock state after surgery. As a medical history, he has chronic kidney disease on hemodialysis, two previous episodes of Pulmonary Embolism (PE) on anticoagulant treatment and chronic IHD secondary to a myocardial infarction (MI) in 2006. After reversal of anticoagulation, he underwent surgery for an arteriovenous peripheral abscess drainage in the left arm. Intraoperatively, there was significant bleeding, estimated as 1 L, due to extension of abscess to deep planes. Two-hours after surgery severe hypotension with tachycardia of 110 bpm and signs of tissular hypoperfusion (lactates of 4.5 mmol/L and ScvO2 63%) occurred.

Step 1: What is the cause of this hemodynamic shock? According to clinical context and medical history it could be the following: (a) hypovolemia secondary to bleeding, (b) septic shock due to abscess, or (c) obstructive shock due to a potential new PE or (d) cardiogenic shock secondary to a new MI.

Step 2: What treatment would you give? (1) Fluid therapy, with its associated risk of overloading as he is patient on hemodialysis; (2) vasopressors, with its associated risk of lowering cardiac output and worsening hypoperfusion; (3) inotropic drugs, with its associated risk of worsening the clinical state if hypovolemia or vasoplegia is the cause of hemodynamic shock.

LV systolic function, observed in the 4-chamber apical view, is estimated to be moderately impaired (LVEF estimated to be around 35%). RV systolic function assessment includes a RV/LV area ratio of 0.9 and a TAPSE of 13 mm measured by M-mode, suggesting a moderate RV systolic dysfunction and mild RV dilatation.

SV is measured by normalized VTI, and a VTI of 21 cm is measured at the LVOT level in the 5-chamber apical view. Fluid responsiveness is assessed by a PLRT and VTI is increased by 13% (from 21 to 24 cm), suggesting that patient is fluid responsive. IVC diameter was 15 mm and distensibility of 20%.

As a summary, this is a patient with a moderately impaired LV systolic function, as well as, a moderately impaired RV systolic function, who is fluid responsive, has a stroke volume of 66 mL estimated by a normalized VTI.

Almost all echocardiographic structural parameters related to perfusion are impaired. Consequently, these values may be confusing.

What echocardiographic perfusion parameters should be prioritized to determine the main contributor to this hemodynamic shock? How to distinguish between chronic or acute impaired perfusion parameters?

Following our algorithm, first step is to determine whether an adequate forward flow is present or not. In this clinical case VTI at LVOT is 21 cm with a HR of 110 bpm, and CO is 7.2L/min. As a result, an adequate SV or forward flow is suggested. Therefore, in the context of hemodynamic shock associated with hypotension, the main contributor is a distributive shock secondary to low systemic vascular resistance (SVR). However, the patient is also fluid responsive with signs of tissular hypoperfusion (lactate 4.5 mmol/L and ScvO2 63%). Therefore, fluid therapy was given first, followed by vasopressors with significant hemodynamics improvement and re-assessment was performed later.

A 42-year-old women, with a perforated duodenal ulcer secondary to NSAIDs required an urgent laparotomy complicated with bleeding. Diffuse secondary peritonitis and severe hemodynamic shock, requiring high dose of noradrenaline (0.4mcg/kg/min), developed postoperatively. She had no past medical history. Biomarkers of infection were increased with a procalcitonin of 20 ng/mL and C-reactive protein of 30 mg/l.

Step 1: What is the cause of this hemodynamic shock? According to clinical context and medical history it could be the following: (a) hypovolemia secondary to bleeding, (b) septic shock due to secondary peritonitis, or (c) obstructive shock due to a PE or (d) cardiogenic shock secondary to a stress cardiomyopathy or a new MI.

Step 2: What treatment would you give? (1) Fluid therapy, with its associated risk of overloading; (2) vasopressors, with its associated risk of lowering cardiac output and worsening hypoperfusion; (3) inotropic drugs, with its associated risk of worsening the clinical state if hypovolemia or vasoplegia is the cause of hemodynamic shock.

24 h postoperatively, an inferolateral elevated ST was observed in ECG. LV global and regional contractility was not impaired and LVOT VTI was preserved (21,5 cm). Few hours later, bigeminy was observed. An anterior, anteroseptal medial and apical akinesia, with a VTI of 14 cm in LVOT and LVEF of 35% was shown in TTE. IVC was 22 mm and distensibility with mechanical ventilation was 5%. Trans-mitral inflow E/A ratio was 1.9. Hypotension and tachycardia (100 bpm) were developed requiring increasing dose of vasopressors and adding vasopressin at 0,03UI/min.

The low VTI of 14 cm associated with a dilated IVC with no distensibility and E/A ratio of almost 2, suggested that the cause of the hemodynamic shock was a mixed distributive and cardiogenic shock due to stress cardiomyopathy, confirmed by a normal coronary angiography.

Dobutamine infusion was initiated at 5 mcg/kg/min and diuretics were given with a significant hemodynamic improvement leading to a decrease of noradrenaline and increase of VTI in LVOT to 17 cm. Dobutamine was stopped 4 days later because LV contractility had recovered and VTI at the LVOT improved (21 cm).

A 65-year-old man with a perforated ascending colon due to a cancer requiring a right colectomy by an urgent laparotomy. Subsequently, a diffuse secondary peritonitis and a hemodynamic shock, requiring high dose of vasopressors (noradrenaline at 0,3mcg/kg/min), was developed. As a medical history, he had hypertension, diabetes, and ischemic cardiomyopathy with preserved LVEF. During surgery bleeding of 1.5 L occurred.

24 h postoperatively, hypotension and tachycardia were progressively increasing requiring increasing dose of vasopressors up to 0,5mcg/kg/min and adding vasopressin at 0,03UI/min, with signs of tissular hypoperfusion (lactate 3,5 mmol/L and ScvO2 64% and oliguria < 0,5 ml/kg/h).

Step 1: What is the cause of this hemodynamic shock? According to clinical context and medical history it could be the following: (a) hypovolemia secondary to bleeding, (b) septic shock due to secondary peritonitis, or (c) obstructive shock due to a PE or (d) cardiogenic shock secondary to a stress cardiomyopathy or a new MI.

Step 2: What treatment would you give? (1) Fluid therapy, with its associated risk of overloading; (2) vasopressors, with its associated risk of lowering cardiac output and worsening hypoperfusion; (3) inotropic drugs, with its associated risk of worsening the clinical state if hypovolemia or vasoplegia is the cause of hemodynamic shock.

TTE showed a not dilated LV with a moderate inferoseptal and inferior hypokinesia. RV was not dilated, and contractility was not impaired. IVC had a diameter of 8 mm with a distensibility of 20%. VTI at LVOT was 16 cm. Trans-mitral inflow E/A ratio was 0.9 suggesting low LV filling pressures. A passive leg raising test was performed and a VTI increased of 15% occurred, suggesting that the patient could benefit from fluid therapy. Hemodynamics improved with the administration of 500 cc of fluid therapy allowing us to decrease noradrenaline dose down to 0,25mcg/kg/min.

The low VTI (16 cm) associated with a small IVC of 8 mm with a distensibility of 20%, along with, low filling pressures with E/A ratio 0.9 and fluid responsive after a PLRT, suggested that the patient was hypovolemic and not yet well filled intravascularly (Table 1).