Respiratory Changes in Aortic Blood Velocity as an Indicator of Fluid Responsiveness in Ventilated Patients With Septic Shock

Feissel. Chest 2001; 119:867-873

Clinical Question

• In patients with septic shock who are mechanically ventilated does indexed LV end-diastolic area or respiratory changes in aortic blood velocity predict the haemodynamic effects of volume expansion?

Design

• Prospective observational diagnostic study
• Presumed convenience sampling (not stated)
• Blinding not stated
• Statistics
  • No sample size calculation performed
  • Nonparametric Wilcoxon rank sum test used to asses the effects of volume expansion on haemodynamic parameters
  • Nonparametric Mann-Whitney test used to compare haemodynamic parameters prior to volume expansion in responder and non-responder patients
  • Linear correlations tested using Spearman rank method

Setting

• 2 intensive care units in France (1 university and 1 non-university)
• Dates of data collection not stated

Population

• Inclusion criteria:
  • Septic shock (defined by 1992 ACCP/SCCM consensus conference)
  • Haemodynamic stability (variation in HR and BP of <10% over the 15 minute period before starting the protocol)
• Exclusion criteria:
  • Arrhythmias, PaO2/FiO2 ratio <100mmHg, contraindication to transoesophageal echocardiography (TOE), aortic valvulopathy, LV systolic dysfunction (fractional area of contraction <30%), doppler LV output recordings using transgastric view could not be obtained
• n=19
  • All received inotropic and vasopressor drugs
  • TOE performed between 12-72 hours after diagnosis of septic shock
  • All had already received colloids (3±2 L) and/or crystalloids (1±1 L)

Tests of Interest

• LV end-diastolic area index (EDAI)
  • TOE used to obtain a transgastric, short-axis, cross-sectional view of the LV at the mid-papillary muscle level
  • End-diastole defined as the frame corresponding to the largest LV cross-sectional area immediately after the R-wave peak on the ECG
  • The anterolateral + posteromedial papillary muscles were included within the ventricular area
  • LV areas divided by body surface area (BSA) to obtain EDAI
  • Used mean of 5 measurements performed at the end of expiration
• Respiratory changes in aortic blood velocity
  • Aortic blood flow measured over single respiratory cycle to allow measurement of peak velocity (Vpeak) and determination of maximum Vpeak values (Vpeakmax) and minimum Vpeak values (Vpeakmin)
  • Change in peak velocity (ΔVpeak %) = [100 * [Vpeakmax – Vpeakmin]] / [[Vpeakmax + Vpeakmin]/2]
  • Mean value of 5 determination used for statistical analysis

Gold standard investigation

• Cardiac output measurement
  • Using TOE, LV outflow tract and ascending aorta imaged when parallel to the ultrasound beam
  • Aortic blood flow measured by pulse wave-doppler at level of aortic valve
  • Diameter of aortic orifice measured at the insertion of the aortic cusp
  • Aortic valve area = π * (aortic diameter/2)
  • Stroke volume = aortic valve area * the velocity time integral of aortic blood flow
  • Cardiac output = stroke volume * heart rate
  • Stroke volume and Cardiac output were divided by the BSA to obtain the stroke volume index and cardiac index
  • If cardiac index increased by ≥15% with fluid challenge classified as responder. If <15% classified as non-responder.
  • Mean of 5 measurements performed at end of expiration used for statistical analysis

Outcome

• Primary outcome: Not defined
• EDAI
  • Before volume expansion
    • No significant difference between responders vs. non-responders
      • 9.7±3.7 vs. 9.7±2.4 cm²/m²
  • Volume expansion led to a significant increase in EDAI
    • 9.7±3.1 cm²/m² to 11.8±3.9 cm²/m²
    • The increase in EDAI significantly correlated with the % increase in Cardiac index (r2 = 0.49, P<0.01) such that the greater the increase in EDAI, the higher the increase in cardiac index in response to volume expansion
• ΔVpeak
  • Before volume expansion
    • Significantly higher in responder vs. non-responder
      • 20±6% vs. 10±3%, P <0.001
    • Using threshold for ΔVpeak of 12%, gave a sensitivity of 100% (95% C.I. 69-100) and specificity of 89% (95% C.I. 52-100) for discriminating between responder and non-responder
      • >12% in all 10 out of 10 responders
      • ≤ 12% in 8 out of 9 non-responders
  • Volume expansion led to a significant decrease in ΔVpeak
    • 15±7% to 8±4%, P<0.001
  • A positive linear correlation found between ΔVpeak before volume expansion and volume expansion-induced changes in cardiac index (r2 = 0.83, P <0.001) i.e. the higher the ΔVpeak before volume expansion, the greater the increase in cardiac index in response to fluid challenge

Authors’ Conclusions

• In patients with septic shock analysis of respiratory changes in aortic blood velocity is an accurate method for assessing fluid responsiveness

Strengths

• Clearly defined test of interest and gold standard investigations
• Tested for inter and intra-observer variability
• Controlled known confounding variables

Weaknesses

• No sample size calculation
• Presumed convenience sample
• Did not state who performed TOE and what training they had received
• Aortic blood velocity used in test of interest and for gold standard investigation
• Small sample size led to wide confidence intervals for sensitivity and specificity

The Bottom Line

• In this small study, patients with septic shock who were mechanically ventilated with tidal volumes of 8-10ml/kg, the respiratory changes in peak aortic blood velocity predicted which patients would have a significant increase in cardiac index with a fluid challenge. The increase in LV end-diastolic area index with a fluid challenge significantly correlated with the increase in cardiac index; where as the baseline LV end-diastolic area index did not predict if a patient would be fluid responsive.

External Links

• [Free full text] Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated patients with septic shock
• [further reading] Life in the Fast Lane: Fluid responsiveness
• [Further reading] ICU Sonography: Tutorial 4 – Volume status and preload responsiveness assessment
• [Further reading] Marik: Echocardiographic Assessment of Preload Responsiveness in Critically Ill Patients
• [Further watching] Ultrasound Podcast: Echo, echo, echo

Metadata

Summary author: David Slessor
Summary date: 7th December 2015
Peer-review editor: Duncan Chambler