A simple algorithm for diferential diagnosis in hemodynamic shock based on left ventricle outfow tract velocity–time integral measurement: a case series
Echocardiography is a procedure that has been used in the critical care setting for a long time. Several working groups from diferent 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. Terefore, echocardiography is often limited to specifc areas such as perioperative cardiac surgery or lung and liver transplantation.
Its use in the cardiology setting has mainly a diagno sis 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 bedside [3, 14–16], such as using mitral Doppler infow 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 illpatients, based on echocardiography [4–6]. Tese echo-cardiographic algorithms focus mainly in its structural perspective and do not ofer a clear guide on how to interpret the fndings in such a complex clinical context, which often leads to starting unnecessary treatment or support measures.
Te aim of this article is to show a simple algorithm based on left ventricle outfow tract (LVOT) velocity–
time integral for diferential diagnosis in hemodynamic shock proposed by the Spanish Critical Care Ultrasound Network Group. Tis algorithm is based on LVOT velocity–time integral measurement, giving a more functional perspective to the use of echocardiography in the critical care setting. Tis functional perspective is based on measuring forward fow, by LVOT velocity–time integralmeasurement, in the LVOT or right ventricle outfowtract (RVOT), which will allow us to measure variables related to perfusion (preload, afterload and contractility).Tis variable integrated into clinical context may have apotential role in the diferential diagnosis for hemodynamic shock in critically ill patients (Fig. 1).
Assessment of hemodynamic status is based on two concepts: perfusion and congestion. Congestion may be assessed by lung ultrasound as well as, hepatic, portalvein and venous renal congestion (VEXUS Score) along with trans-mitral infow and E/e’ ratio to estimate LV flling pressures. However, in our article, we will focus on perfusion parameters rather than congestion.
Our review will be centered on transthoracic echocar-diography, although it might also be used by transesoph-ageal 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 diferential diagnosis and management of the hemodynamic shock.
Clinical case 1
Tis 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 hypov
olemia 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 fow (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-infow E/A ratio was 1.2.
The VTI of 19 cm, calculated by TTE, helped us in our diferential 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 fuids.
Clinical case 2
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 signifcant 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) Fluidtherapy, 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 RVdilatation.
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 fuid 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 fuid 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, frst step is to determine whether an adequate forward fow 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 fow is suggested. Terefore, 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 fuid responsive with signs of tissular hypoperfusion (lactate 4.5 mmol/L and ScvO2 63%). Terefore, fuid therapy was given frst, followed by vasopressors
with signifcant hemodynamics improvement and reassessment was performed later.
Clinical case 3
A 42-year-old women, with a perforated duodenal ulcer secondary to NSAIDs required an urgent laparotomy complicated with bleeding. Difuse 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 infow 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, confrmed by a normal coronary angiography.
Dobutamine infusion was initiated at 5 mcg/kg/min and diuretics were given with a signifcant 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).
Clinical case 4
A 65-year-old man with a perforated ascending colon due to a cancer requiring a right colectomy by an urgent laparotomy. Subsequently, a difuse 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, andischemic cardiomyopathy with preserved LVEF. Duringsurgery bleeding of 1.5 L occurred.
24 h postoperatively, hypotension and tachycardia wereprogressively increasing requiring increasing dose ofvasopressors 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 couldbe 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 shocksecondary 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 outputand worsening hypoperfusion; (3) inotropic drugs, withits 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 diameterof 8 mm with a distensibility of 20%. VTI at LVOT was16 cm. Trans-mitral infow E/A ratio was 0.9 suggestinglow LV flling pressures. A passive leg raising test wasperformed and a VTI increased of 15% occurred, suggesting that the patient could beneft from fuid therapy.Hemodynamics improved with the administration of500 cc of fuid therapy allowing us to decrease noradrenaline dose down to 0,25mcg/kg/min.
The low VTI (16 cm) associated with a small IVC of8 mm with a distensibility of 20%, along with, low fllingpressures with E/A ratio 0.9 and fuid responsive after aPLRT, suggested that the patient was
hypovolemic and not yet well flled intravascularly (Table 1).
In this article, a case series of patients have been reportedto whom the algorithm based on LVOT velocity–timeintegral measurement was performed, and its use wascrucial for diferential diagnosis and management ofhemodynamic shock.
For the assessment of perfusion, it is essential to measure the CO. CO calculation often justifes the use ofinvasive monitors such as the pulmonary artery catheterpulmonary (PAC) or other transpulmonary thermodilution-based systems.
CO calculation by echocardiography non-invasivelyhas been compared to thermodilution by the pulmonary artery catheter (PAC), showing an excellent performance. Data from a prospective cohort study on 50cardiac surgery patients determining the correlationbetween ultrasound (US) and PAC, showed an excellentperformance to detect a 10% variation in CO (Receiveroperating curve (ROC 0.9; specifcity 71% and sensitivity 92%) . More recently, data from a meta-analysis on1,996 patients from 68 studies, no signifcant diferenceswere found between US and thermodilution-derived CO(mean diference− 0.14; 95% CI− 0.30 to 0.02;p=0.08).
Cardiac ultrasound allows calculating SV by usingpulsed wave Doppler (PWD) technique. PWD calculatesthe velocity of red blood cells at a specifc point in thecardiovascular system. If PWD is applied at the level ofthe LVOT, a triangular image will be obtained that represents the spectrum of velocities of the red blood cells thatpass through this point during each beat.
If the surface of such a triangle is traced with ourultrasound system, the VTI, will be obtained, which isexpressed in cm (Fig. 2).
VTI is the length of the column of blood passingthrough a single point in each heartbeat. It is consideredthat the LVOT is a circular structure that does not signifcantly change its shape during the cardiac cycle.
The volume of blood ejected from the left ventricleduring systole passes through the LVOT, which is shapedlike a cylinder. Solving for the volume of that cylinder,therefore, yields the SV (Fig. 2):
Cylinder volume = height × CSA,
where CSA indicates the cross-sectional area. Te heightof the cylinder is the LVOT VTI, obtained by pulsed wave(PW) Doppler placed just proximal to the aortic valve inan apical fve- or three-chamber view.
The SV may be calculated by multiplying VTI by thecross-section area (CSA) at the level of LVOT: CSA=Π×(diameter LVOT/2) . Te main limitation withthis measurement is that calculation of LVOT diameter (LVOTd) is a measurement with poor reproducibility. Consequently, when interpreting the progression ofthe CO, it is unknown whether the changes are relatedto treatment or diferences in the LVOTd measurement.A well acquired LVOT VTI is represented by a spectralenvelope, which is “dark” on the inside with a bright “outline.” LVOT VTI should include the closure "click" of theaortic valve in the Doppler profle.
It was chosen to convert the LVOT in a constantparameter, given that, it is a value that does not changesignifcantly over time and is proportional to body surface area (BSA) . Tis simplifcation allows us toassume that SV=VTI. Terefore, the changes in VTIrefect changes in the SV. Tis has already been mentioned in a consensus document on monitoring in hemodynamic shock by a working group from the ESICM .
In this way, it is possible to estimate SV by normalizing the LVOTd to the global population mean, LVOTd of2 cm (20.3±2.3 mm) [9,11–13].If the LVOTd is normalized, assuming the globalpopulation mean, the following formula may be used:SV=VTI×[Π×(2/2)2]=VTI×Π (=3.14).Based on this formula, SV may be calculated based onVTI values. A calculated VTI of 18 cm, corresponds toan SV of 56.5 mL, which is very close to 60 mL, which isthe lower limit of normality, according to hemodynamicliterature and the cut-of value to defne a low SV (Fig. 3).A VTI of 18 cm has been used as the cut-of value forlow SV for several reasons. First, it is assumed that thereis a tendency to underestimate the VTI, due to a suboptimal Doppler bean alignment between our beam and theorientation of the LVOT. Tus, it is possible to assess perfusion using VTI directly, either in the LVOT or RVOT[12–14]. Second, guidelines from the American Societyof Echocardiography (ASE) for the echocardiographyas a monitor for therapeutic intervention in adults suggest VTI>18 cm, as an adequate CO . Tis suggestion is based on data from an observational cohort studyon 990 ambulatory patients with stable coronary arterydisease (CAD), where it is observed that a VTI<18 cm isassociated with an increase rate of heart failure requiringhospitalization and mortality independent of clinical andother echocardiographic parameters .A recent editorial was emphasizing and suggesting thathemodynamic monitoring is best achieved with the use ofa simple quantitative measurement refecting stroke volume—VTI at the LVOT or RVOT—and that this measurement should be taught to every operator at the earlieststage of echo training. Te author suggested that since fowis such a crucial indicator of tissue perfusion and the targetof most of our therapeutic interventions, it seems reasonable to include LVOT VTI measurement in the curriculumof “basic” echo training . Tis approach has also beensupported by other experts in the feld of critical care echocardiography . Te view to be used for LVOT VTI isapical 5-chamber or apical 3-chamber view. PWD at theLVOT, 1 cm proximal to the aortic valve, should be usedto measure VTI. As already mentioned above, the valueof 18 cm is the minimum normal value of VTI, which discriminates between normal or low SV.
The average overall RVOT distal diameter is slightlylarger than LVOTd (21.7±3.14 mm vs 20.3±2.3 mm) .Terefore, the RVOT VTI cut-of value should be slightlylower (from 18 to 15 cm) than LVOT VTI. Te view to beused for RVOT VTI is subcostal short-axis RVOT or parasternal long-axis RV outfow. Tis value as the cut-ofvalue should be interpreted into clinical context. Critical care setting is complex, but for the sake of simplicityit is useful to have a clear fgure in memory to serve as areference.
The main limitations for using VTI as SV calculation arethe following:
1. SV calculation will be overestimated if the following pathologies are present: (a) subaortic stenosis,(b) LVOT dynamic obstruction associated with systolic anterior motion (SAM), (c) moderate-to-severeaortic regurgitation, and (d) the presence of aorticprosthetic valve. To overcome this limitation, measurement of VTI at the RVOT, placing the PWD justbefore the pulmonary valve, by the subcostal shortaxis RVOT or parasternal long-axis RV outfow, maybe used.
2. Either a smaller (SV will be overestimated) or larger(SV will be underestimated) LVOT diameter thanmean global population in people with low or highbody surface area (BSA). To overcome this limitation,the LVOTd should be measured by an expert sonographer.
VTI‑based algorithm in hemodynamic shock proposal
In this article, an algorithm based on LVOT velocity–timeintegral measurement it is proposed by the Spanish CriticalCare Ultrasound Network Group, for hemodynamic shockassessment, guiding in the decision-making for diferentialdiagnosis (Fig. 4).First step is to analyze whether the patient has an adequate forward fow in terms of SV and CO. Tis frst stepwill be answered by the measurement of the normalizedVTI at LVOT or RVOT:1. If VTI is above 20 cm, the SV is adequate and therefore the cause of the hemodynamic shock will mostlikely be a distributive shock. In this case, after initiating vasopressors to normalized mean blood pressure, VTI will be reassessed to ensure SV has not beenreduced by increasing afterload related to vasopressors.2. On the other hand, if VTI is below 16 cm, an abnormally low SV is suggested, and the cause of this lowcardiac output syndrome should be diagnosed. Telower limit of VTI has been downgraded to 16 cmbecause most of the time in critical care, imagesobtained are less than optimal and there is a tendencyto underestimate the VTI, due to a suboptimal Doppler bean alignment. Terefore, VTI between 18±2is left as a “gray-zone” where clinical assessment is ofparamount importance.2.1First, pericardial function is evaluated to rule outcardiac tamponade.2.2 Second, RV systolic function and size will be evaluated. If RV systolic function is impaired or severeRV dilatation is present, the most likely cause of thehemodynamic shock is obstructive shock, e.g., massive pulmonary embolism (PE), and it may be treatedaccordingly. However, diferential diagnosis includesother causes of RV pressure or volume overload, suchas acute cor pulmonale (ARDS, COPD, asthma), tension pneumothorax, RV infarction, decompensatedchronic pulmonary hypertension (PHTN), fuid overload or stress-related RV systolic impairment (sepsiscardiomyopathy).2.3Tird, if RV systolic function is normal, LV systoliccontractility will be assessed by eyeballing. LV flling pressure will be measured by mitral-infow E/Aratio. If LV systolic function is moderate or severelyimpaired, in absence of hypovolemia, the most likelycause is cardiogenic shock, including diastolic dysfunction, sepsis stress-cardiomyopathy, MI, decompensated previous cardiomyopathy, myocarditis.2.4Fourth, if massive mitral or aortic regurgitation isobserved, it could be a main contributor of the hemodynamic shock.2.5Lastly, fuid responsiveness will be assessed. Ifpatient is responsive, fuid therapy will be given.Te order followed for the perfusion parameters assessment in our algorithm is not trivial. Te goal is to recoverperfusion parameters without over resuscitating thepatient avoiding adverse efects. For this reason, fluid
responsiveness is the last one to be evaluated, after rulingout tamponade, RV/LV systolic function and left-sided valvular incompetency.To achieve this goal, our premise is the following: astructural cardiac dysfunction does not signifcantly contribute to the hemodynamic shock, unless causes a lowcardiac output syndrome, measured by a normalizedVTI below 16 cm. Terefore, it should not be treated.Even if the patient is fuid responsive and VTI is normal(VTI>18 cm), fuid therapy may not be recommended,unless signs of tissular hypoperfusion are present. Tis isthe normal physiological state and if SV is not low, fuidtherapy may lead to worse outcomes associated withadverse efects secondary to overloading [19–21].Te presence of regional or global wall motion abnormalities does not necessarily mean it should be treatedwith inotropic support unless low SV (VTI<18 cm)occurs. Inotropic support is indicated for low-cardiacoutput syndrome associated with signs of tissular hypoperfusion unless you have LV or RV outfow obstruction.Te use of inotropic support in a patient with an adequate SV (VTI>18 cm) might lead to an increased myocardial mechanical stress and oxygen consumption withits risk of arrhythmias.Te presence of RV contractility impairment or RVdilatation associated with an adequate SV (VTI>18 cm)means that the RV dysfunction is not the cause of hypotension or hemodynamic shock. As an example, if apatient is diagnosed of PE in the clinical context of hemodynamic shock with normal SV, the RV dysfunction will,most likely, not be the main cause of shock. It wouldrather be a distributive shock, requiring to rule out septicshock and controlling its source.Overall, if there is no beneft from using a specifctreatment, it should be avoided to decrease its associatedadverse efects.Our algorithm is not intended to be an algorithm thatfts all possible clinical scenarios, since it would be toolong and therefore not useful at the clinical level. Tension pneumothorax and LVOT/RVOT obstruction wouldbe fuid responsive. However, they are out of the scopeof our algorithm. Combined RV and LV systolic impairment would include both clinical scenarios. Abdominalcompartment syndrome would not be included in ouralgorithm.Te measurement of LV flling pressure by mitralinfow E/A ratio > 2 could only be used when LV systolic function impairment exists. Furthermore, onlyE/A > 2 and E/A < 0.8+E velocity < 0.5 m/s can beused in isolation to clearly defne LV flling pressurein those patients. Te range of E/A 0.8—2.0 is indeterminate and required to measure additional variables(left atrium size, E/E’ ratio and tricuspid regurgitationpeak velocity). Also, LV flling pressure can be normalwith an E/A > 2 in patients with normal diastolic function (young < 40 years old). Te criteria to accuratelyassess fuid responsiveness by aortic valve peak velocity or VTI variation associated with invasive mechanical ventilation are well known: (a) sinus rhythm withno premature atrial or ventricle contraction; (b) tidalvolume > 7 ml/kg; (c) absence of inspiratory eforts andlastly, but more importantly, absence of RV systolicdysfunction.IVC distensibility test requires the following criteria toperform well: (a) tidal volume>=8 ml/kg; (b) PEEP nomore than 5; (c) absence of inspiratory eforts or assistedpressure support; (d) absence of moderate-to-severe tricuspid regurgitation or RV dysfunction; (e) absence ofintra-abdominal hypertension and, lastly, absence of cardiac tamponade.It is proposed as a mental guide to prioritize conceptsand facilitate the integration of echocardiography intopatient’s clinical context for clinical decision-making.To conclude, several topics will be discussed for thealgorithm to perform well:
– Once the treatment has been applied, echocardiographic re-assessment to confrm SV improvementshould be performed. Reassessment is also crucialwhen a signifcant hemodynamic change occurs (e.g.,tachycardia, increase need for vasopressors/inotropes and hypoperfusion refractory to treatment).– Clinical situations where VTI is in the “gray-zone”(VTI between 16 and 20), it is crucial the clinicalcontext and tissue perfusion assessment by measurement of arterial lactate, central venous oxygen saturation, CO2 venous–arterial gradient. If hypoperfusion persist, despite having optimized oxygen arterialsaturation and hemoglobin, measures to increase SVshould be applied. Te “gray-zone” of VTI between16 and 20 cm could be debated. Sattin et al.  haverecently suggested a systematic approach for usingSV measurements to help integrate important 2Dfndings into the clinical context. Tey proposed a“gray-zone” of VTI between 14 and 22 cm, suggesting to measure the LVOTd in case of a VTI in the“gray-zone” between 14 and 22 cm. However, LVOTdmeasurement has poor reproducibility. Any smallerror in measuring the LVOTd may lead to a signifcant overestimation or underestimation of the SV.Terefore, we suggest that only experienced sonographers perform LVOTd measurement. Te average overall RVOT distal diameter is slightly largerthan LVOTd (21.7±3.14 mm vs 20.3±2.3 mm) .
Terefore, the RVOT VTI cut-of value should beslightly lower (from 18 to 15 cm) than LVOT VTI.– If tachycardia is present, it should be evaluatedwhether it is a compensatory or a reactive tachycardia. Compensatory tachycardia is secondary to alow CO syndrome (e.g., cardiogenic, obstructive, orhypovolemic shock), whereas a reactive tachycardiais secondary to an infammatory state such as distributive shock (e.g., Sepsis or Systemic InfammatoryResponse Syndrome—SIRS), associated with a normal or high CI>2.5 L/min/m2. If CI is<2.2 L/min/m2, compensatory tachycardia is suggested and treatment to increase SV either with fuids or inotropes,should be applied.– If AF is present, the mean of fve VTI measuresshould be used for a normalized VTI and CI calculation.
In this article, a case series of patients have been reportedto whom the algorithm based on LVOT velocity–timeintegral measurement was performed and its use wascrucial for diferential diagnosis and management ofhemodynamic shock.Tis simple algorithm aims for guiding in the decisionmaking for the diferential diagnosis of hemodynamicshock. It represents a shift in the classic hemodynamicshock assessment and management guide by echocardiography. Tis shift consists of moving from a morestructural perspective to a more functional one. Ourfunctional perspective aims for integrating all perfusion parameters through a simple algorithm, rather thanevaluating structural abnormalities separately, with nointegration into a functional assessment. Ultimately, it isa useful tool for individualizing treatment, detecting themain contributor to the hemodynamic shock state, followed by an early appropriate treatment, avoiding fuidoverloading or inotropes overuse. Whether the use ofthis simple algorithm VTI-based in hemodynamic shockmay improve important clinical outcomes remains to beelucidated.
AF: Atrial fbrillation; AMI: Acute myocardial infarction; ARDS: Acute respiratorydistress syndrome; ASE: American Society of Echocardiography; BP: Bloodpressure; BSA: Body surface area; CAD: Coronary artery disease; CI: Cardiacindex; CO: Cardiac output; CSA: Cross-sectional area; CVP: Central venouspressure; HR: Heart rate; IVC: Inferior vena cava; LVEF: Left ventricle ejectionfraction; LVOT: Left ventricle outfow tract; MAP: Mean arterial pressure; P1:Pressure 1; P2: Pressure 2; PAC: Pulmonary artery catheter; PE: Pulmonaryembolism; PLRT: Passive leg raising test; PWD: Pulse wave Doppler; RVOT:Right ventricle outfow tract; SAM: Systolic anterior motion; SIRS: Systemicinfammatory response syndrome; SV: Stroke volume; SVR: Systemic vascularresistance; TEE: Transesophageal echocardiography; TTE: Transthoracic echo‑cardiography; US: Ultrasound; VTI: Velocity–time integral.
WBS is supported by the KRESCENT program of the Kidney Foundation ofCanada and the Fond de Recherche du Québec en Santé (Clinical ScholarJunior 1). Spanish Critical Care Ultrasound Network Group: Marc Vives5, AlbertoHernández2, Duilio González-Delgado5, PaulaCarmona6, XavierBorrat1, DavidNagore7, Eduardo Sánchez8, MariaSerna9, PabloCuesta10, Unai Bengoetxea11,FranciscoMiralles12and Jordi Mercadal11Department of Anesthesiology & Critical Care. Hospital Clinic. University ofBarcelona. Spain2Department of Anesthesiology & Perioperative Medicine, Policlinica IbizaHospital, Ibiza, Spain5Department of Anesthesiology & Critical Care. Clínica Universidad de Navarra.Universidad de Navarra. Spain6Department of Anesthesiology & Critical Care. Hospital Universitario y Politéc‑nico La Fe. Valencia, Spain7Department of Anesthesiology & Critical Care. Barts Heart Centre, St Bartho‑lomew’s Hospital, London, UK.8Department of Anesthesiology & Critical Care. Hospital Universitario GregorioMarañon. Madrid, Spain9Department of Anesthesiology & Critical Care. Hospital Universitario deAlicante. Alicante, Spain10Department of Anesthesiology & Critical Care. Hospital Universitario deAlbacete. Albacete, Spain11Department of Anesthesiology & Critical Care. Hospital Urduliz. Urduliz, Spain12Department of Anesthesia & Surgery Critical Care Service, Hospital Universi‑tario Puerta del Mar, Cádiz, Spain.
All authors have contributed intellectually to the work, meeting the condi‑tions of authorship, and have approved the fnal version of the article. Allauthors read and approved the fnal manuscript.
No funding was needed.
Availability of data and materials
The datasets used and/or analyzed during the current study are available fromthe corresponding author on reasonable request.
Ethics approval and consent to participateThe need for ethics approval was waived.
Consent for publication
Written informed consent was obtained from the patients for publication ofthis case report.
No fnancial and non-fnancial competing interests exist.
1Department of Anesthesiology & Critical Care, Hospital Clinic, Universityof Barcelona, Barcelona, Spain.2Department of Anesthesiology & PerioperativeMedicine, Policlinica Ibiza Hospital, Ibiza, Spain.3Department of Anesthesiaand Intensive Care Unit, Research Centre, Montreal Heart Institute and Uni‑versité de Montréal, Montreal, QC, Canada.4Division of Nephrology, CentreHospitalier de L’Université de Montréal, Montreal, Canada.5Departmentof Anesthesiology & Critical Care, Clínica Universidad de Navarra, Universidadde Navarra, Av. Pio XII, 36. 31008 Pamplona, Navarra, Spain.
Received:9 May 2022 Accepted: 3 Auqust 2022
Published online: 24 August 2022